Phage , the virus that cures

[William Gaatjes]

More proof about the symbiotic connection between the bacteria in our gut and the host. This research is about how the composition of bacteria species and activity of these bacteria alters when the host has a non circadian rhythm. Also, there is more proof that the gut composition and activity of bacteria has a serious effect on the health of the host.
It seems that the bacteria synchronize their activity to the hosts eating patterns. Thus it seems, eating when the host should be sleeping is a no go. Eating at fixed times when awake is the best way to prevent diseases.
Very difficult for people who frequently fly from one timezone to another.

http://news.sciencemag.org/biology/2014/10/are-your-bacteria-jet-lagged?rss=1

Life on Earth is intimately connected to the natural cycles of light and dark that make up a 24-hour day. For plants, animals, and even bacteria, these circadian rhythms control many biological functions. Humans can overrule their body clocks, but at a price: People whose circadian rhythms are regularly disrupted—by frequent jet lag or shift work, for example—are more vulnerable to diabetes, obesity, cardiovascular disease, and cancer. There are various theories to explain these associations, and researchers now have a new player to consider: the bacteria that live in the digestive tract. According to a study in mice and a small group of human volunteers, the internal clocks of these gut microbes sync up with the clocks of their hosts. When our circadian rhythms get out of whack, so do those of our bacteria.

The last several years have seen an explosion of interest in the constellation of bacteria that call the gut home, and these microbes appear to play a role in everything from immunity to metabolism to mood. But although disrupted bacteria are observed in many of the same diseases that arise from skewed circadian rhythms, the precise link isn’t fully understood. Eran Elinav, an immunologist and microbiome specialist at the Weizmann Institute of Science in Rehovot, Israel, wondered whether the microbes’ own circadian rhythms were a missing piece of the puzzle.

To test the theory, he and his colleagues analyzed bacteria in fecal samples from lab mice kept in normal 12-hour cycles of light and darkness. Samples were taken every 6 hours for two 24-hour cycles. Up to 60% of the microbes consisted of various bacterial types that fluctuated, in both their total number and their prevalence relative to each other, throughout the day and night. During the dark phase (when mice, being nocturnal, are most active), the bacteria were busy digesting nutrients, repairing their DNA, and growing, as evidenced by the various bacterial gene activity documented from fecal samples taken at different time points. During the light phase, microbes went about ongoing "housekeeping" processes, such as detoxifying, sensing the chemicals around them, and building the flagella, or tails, that help the microbes move.

In mice with a mutation that disables the inner clock, the gut bacteria didn’t exhibit the same fluctuations, in either population or activity, in response to light and dark—suggesting that the animal's clock somehow controls that of the bacteria. When bacteria from these "clockless" mice were transplanted into healthy animals living in normal light-dark conditions, the microbes began to show normal rhythms within a week.

The findings, reported online yesterday in Cell, came as a surprise, Elinav says. Previous studies have shown that many bacteria do have light-responsive circadian clocks—cyanobacteria, for example, which get their energy from photosynthesis. But microbes deep in the bowels of—well, the bowels—spend all their time in the dark. How did they know what time of day it was? Some signal must pass from the host to the bacteria.

One major difference between normal mice and clock-disabled ones was the time at which the animals ate, the researchers observed. Normal mice eat at night, while they're active; the clockless mice ate almost continuously. So could the timing of meals be the signal? When the researchers altered the animals' eating patterns by feeding normal mice only during the light cycle (a mouse's night), the numbers, types, and activity of the bacteria shifted as well. The researchers also found that mice whose light-dark cycles were disrupted gained weight and developed physiological changes linked to diabetes, such as insulin resistance. Because humans with irregular sleeping patterns also tend to eat more at night, the researchers suspect that these eating habits contribute to disease specifically by disrupting the gut microbes.

Bacteria are likely not the whole story; irregular sleeping and eating can contribute to disease through other routes, such as excess stress hormone and insulin production. Even so, "this is a compelling study," says microbiologist Rob Knight of the University of Colorado, Boulder. Knight says some of the strongest evidence for a bacterial role in circadian-linked diseases lies in the final phase of the study, when the research team analyzed fecal samples from two people on a normal schedule and two more who had recently flown from the United States to Israel. Analyzing the samples before, during, and after the bouts of jet lag, they found fluctuations in bacteria similar to what they saw in the mice. The jet-lagged participants showed an increase in a type of bacteria known to be more prevalent in people with obesity and diabetes; levels of these microbes dropped back to normal once the travelers adjusted to the new time zone.

Most convincing of all, Knight believes, is that when samples of gut bacteria from the jet-lagged humans were transplanted into healthy mice, the animals gained weight, showed increased blood sugar, and had a higher body fat content compared with animals given the bacteria of participants before their flight.

So can we ward off the ill effects of jet lag by being more careful about how or when we eat? At this point, "it's an educated guess," Elinav says.

 

[William Gaatjes]

I was wondering regarding post 276 what the effects would be of drugs abuse on the gut bacteria. For example cocaine, crack cocaine and crystal meth cause serious sleeping disorders. Leaving addicts awake for many days. Other then that, addicts who do not eat regularly, it would make sense that these people people have also a different gut bacteria composition. Perhaps that a part of the addiction can also be explained by the gut bacteria composition and activity and the resulting effects on the neurons in the gut and in the end the nervous system and brain.

It may be unrelated, but i doubt it...
If memory serves me right, 95 percent percent of all the serotonin in the body resides in the gut and not in the brain as many (including me once long ago) would think.

One poster in this thread mentioned the second brain long ago.

http://www.scientificamerican.com/article/gut-second-brain/

As Olympians go for the gold in Vancouver, even the steeliest are likely to experience that familiar feeling of "butterflies" in the stomach. Underlying this sensation is an often-overlooked network of neurons lining our guts that is so extensive some scientists have nicknamed it our "second brain".

A deeper understanding of this mass of neural tissue, filled with important neurotransmitters, is revealing that it does much more than merely handle digestion or inflict the occasional nervous pang. The little brain in our innards, in connection with the big one in our skulls, partly determines our mental state and plays key roles in certain diseases throughout the body.

Although its influence is far-reaching, the second brain is not the seat of any conscious thoughts or decision-making.

"The second brain doesn't help with the great thought processes…religion, philosophy and poetry is left to the brain in the head," says Michael Gershon, chairman of the Department of Anatomy and Cell Biology at New York–Presbyterian Hospital/Columbia University Medical Center, an expert in the nascent field of neurogastroenterology and author of the 1998 book The Second Brain (HarperCollins).

Technically known as the enteric nervous system, the second brain consists of sheaths of neurons embedded in the walls of the long tube of our gut, or alimentary canal, which measures about nine meters end to end from the esophagus to the anus. The second brain contains some 100 million neurons, more than in either the spinal cord or the peripheral nervous system, Gershon says.

This multitude of neurons in the enteric nervous system enables us to "feel" the inner world of our gut and its contents. Much of this neural firepower comes to bear in the elaborate daily grind of digestion. Breaking down food, absorbing nutrients, and expelling of waste requires chemical processing, mechanical mixing and rhythmic muscle contractions that move everything on down the line.

Thus equipped with its own reflexes and senses, the second brain can control gut behavior independently of the brain, Gershon says. We likely evolved this intricate web of nerves to perform digestion and excretion "on site," rather than remotely from our brains through the middleman of the spinal cord. "The brain in the head doesn't need to get its hands dirty with the messy business of digestion, which is delegated to the brain in the gut," Gershon says. He and other researchers explain, however, that the second brain's complexity likely cannot be interpreted through this process alone.

"The system is way too complicated to have evolved only to make sure things move out of your colon," says Emeran Mayer, professor of physiology, psychiatry and biobehavioral sciences at the David Geffen School of Medicine at the University of California, Los Angeles (U.C.L.A.). For example, scientists were shocked to learn that about 90 percent of the fibers in the primary visceral nerve, the vagus, carry information from the gut to the brain and not the other way around. "Some of that info is decidedly unpleasant," Gershon says.

The second brain informs our state of mind in other more obscure ways, as well. "A big part of our emotions are probably influenced by the nerves in our gut," Mayer says. Butterflies in the stomach—signaling in the gut as part of our physiological stress response, Gershon says—is but one example. Although gastrointestinal (GI) turmoil can sour one's moods, everyday emotional well-being may rely on messages from the brain below to the brain above. For example, electrical stimulation of the vagus nerve—a useful treatment for depression—may mimic these signals, Gershon says.

Given the two brains' commonalities, other depression treatments that target the mind can unintentionally impact the gut. The enteric nervous system uses more than 30 neurotransmitters, just like the brain, and in fact 95 percent of the body's serotonin is found in the bowels. Because antidepressant medications called selective serotonin reuptake inhibitors (SSRIs) increase serotonin levels, it's little wonder that meds meant to cause chemical changes in the mind often provoke GI issues as a side effect. Irritable bowel syndrome—which afflicts more than two million Americans—also arises in part from too much serotonin in our entrails, and could perhaps be regarded as a "mental illness" of the second brain.

Scientists are learning that the serotonin made by the enteric nervous system might also play a role in more surprising diseases: In a new Nature Medicine study published online February 7, a drug that inhibited the release of serotonin from the gut counteracted the bone-deteriorating disease osteoporosis in postmenopausal rodents. (Scientific American is part of Nature Publishing Group.) "It was totally unexpected that the gut would regulate bone mass to the extent that one could use this regulation to cure—at least in rodents—osteoporosis," says Gerard Karsenty, lead author of the study and chair of the Department of Genetics and Development at Columbia University Medical Center.

Serotonin seeping from the second brain might even play some part in autism, the developmental disorder often first noticed in early childhood. Gershon has discovered that the same genes involved in synapse formation between neurons in the brain are involved in the alimentary synapse formation. "If these genes are affected in autism," he says, "it could explain why so many kids with autism have GI motor abnormalities" in addition to elevated levels of gut-produced serotonin in their blood.

Down the road, the blossoming field of neurogastroenterology will likely offer some new insight into the workings of the second brain—and its impact on the body and mind. "We have never systematically looked at [the enteric nervous system] in relating lesions in it to diseases like they have for the" central nervous system, Gershon says. One day, perhaps there will be well-known connections between diseases and lesions in the gut's nervous system as some in the brain and spinal cord today indicate multiple sclerosis.

Cutting-edge research is currently investigating how the second brain mediates the body's immune response; after all, at least 70 percent of our immune system is aimed at the gut to expel and kill foreign invaders.

U.C.L.A.'s Mayer is doing work on how the trillions of bacteria in the gut "communicate" with enteric nervous system cells (which they greatly outnumber). His work with the gut's nervous system has led him to think that in coming years psychiatry will need to expand to treat the second brain in addition to the one atop the shoulders.

So for those physically skilled and mentally strong enough to compete in the Olympic Games—as well as those watching at home—it may well behoove us all to pay more heed to our so-called "gut feelings" in the future.

 

[William Gaatjes]

This is interesting.
From what i understand about it :
The CRISPR/Cas system is a technique that prokaryotic cells use to repair dna damage. When a bacteria gets infected by a virus and that virus "installs" its dna into the bacterial virus, the bacteria have a way to remove that dna. The CRISPR/Cas system is simply put (but not really) the immune system of the bacteria.
It recognizes hostile dna and then it is able to detect that hostile dna already inserted into the host dna and removes it again.

If you want to know more : http://en.wikipedia.org/wiki/CRISPR

But for a while scientists are now able to use this system to even remove (viral) dna from human cells or to add dna to human cells.
This is just one of many papers that have emerged about using this system.

http://arstechnica.com/science/2015/03/new-dna-construct-can-set-off-a-mutagenic-chain-reaction/

New DNA construct can set off a “mutagenic chain reaction”

A technique for editing genes while they reside in intact chromosomes has been a real breakthrough. Literally. In 2013, Science magazine named it the runner-up for breakthrough-of-the-year, and its developers won the 2015 Breakthrough Prize.

The system being honored is called CRISPR/Cas9, and it evolved as a way for bacteria to destroy viruses using RNA that matched the virus' DNA sequence. But it's turned out to be remarkably flexible, and the technique can be retargeted to any gene simply by modifying the RNA. Researchers are still figuring out new uses for the system, which means there are papers coming out nearly every week, many of them difficult to distinguish.

Bacterial “immune system” used to engineer human DNA in human cells
System lets researchers target changes to specific sites in the genome.

That may be precisely why the significance of a paper published last week wasn't immediately obvious. In it, the authors described a way of ensuring that if one copy of a gene was modified by CRISPR/Cas9, the second copy would be—useful, but not revolutionary. What may have been missed was that this process doesn't stop once those two copies are modified. Instead, it happens in the next generation as well, and then the generation after that. In fact, the modified genes could spread throughout an entire species in a chain reaction, a fact that has raised ethical and safety concerns about the work.
New developments

The CRISPR/Cas9 system is remarkably simple. It relies on RNA molecules that have a specific format and are able to base pair with a site in the genome. Cas9 then cuts the DNA at the site where this base pairing occurs, creating a break in the chromosome. Cells have systems that attempt to repair these breaks, and these systems attempt to identify similar-looking sequences to use as a template for repair. So if you provide the cells with some similar DNA, it will end up being placed at the site that the RNA first targeted.

This makes it easy to modify the genome. By providing slightly different DNA to be used in the repair process, you can substitute altered bases, short deletions, or even entire additional genes, any of which can take their place within the chromosome. In short, CRISPR/Cas9 lets you put any DNA you want anywhere in a genome.

It's possible to use this to eliminate genes you're interested in, so you can study animals that lack that gene. You simply target the gene with an RNA, and then provide DNA with a deletion of a key part of the gene. The repair system will use the deletion as part of its template and copy it into place on the chromosome. It's also possible to mutate a gene by replacing key parts of it with something else. For example, you could swap in a copy of the Green Fluorescent protein and ensure that all of the resulting mutants glow green.

But you still have to breed these mutations the old-fashioned way: you need to get two organisms that have a copy of the mutant gene, then breed them together. Mendel then tells us that one-quarter of the offspring will have mutant copies in both of their chromosomes.

The authors of the new paper found that frustratingly slow. Working in flies, they designed a system where CRISPR/Cas9 would do all the work for them. Their DNA repair template was a bit more complicated than a simple deletion. Instead, it contained the genes needed to get the CRISPR/Cas9 system to work, along with a guide RNA that targeted a specific fly gene (in this case, yellow). They surrounded all these genes with DNA from the yellow gene itself.

Once injected in the fly, the normal yellow gene was disrupted by the genes for the CRISPR/Cas9 system. Once that happened on one chromosome, the system could easily perform the same modification on the other chromosome, making the animal a homozygous yellow mutant.

But the key thing is what happens in the next generation. In these animals, a normal copy of the yellow gene comes in from the next parent. But the CRISPR/Cas9 cassette immediately converts that, too, resulting in offspring that are all yellow. Well, not all; but the authors found that the construct was 97 percent effective at converting the next generation. In fact, there's nothing to stop this system from invading an entire population, continuing to convert generation after generation until everything carries the modification.

It's a bit like the futurists' fears of a self-perpetuating "grey goo," just played out with yellow-colored flies. (For those of you with a biology background, this will also sound a lot like an engineered homing intron.)
Precautions

Fortunately, the researchers were conscious of the issues: "we are also keenly aware of the substantial risks associated with this highly invasive method since the failure to take stringent precautions could lead to the unintentional release of [modified] organisms into the environment." The flies were bred behind three layers of containment in a locked facility. The containers were put straight into the freezer to kill the flies if they were no longer needed. Any manipulations of the flies were performed while they were anesthetized in a Biosafety Level 2 facility.

Still, there are further precautions that could be taken. The report cites a draft manuscript, hosted on the bioRxiv, that describes a similar system in yeast. In this case, however, only the targeting RNA is inserted into the targeted gene—the rest of the CRISPR/Cas9 system has to be provided separately for anything to happen. One of the authors of this manuscript, the synthetic biologist George Church, told a Science reporter that he felt the fly work should never have been published because the technology was too dangerous.

Why do the work at all if it's so risky? Because, properly controlled, there could be some amazing benefits. Imagine using it to quickly breed traits from non-agricultural plants (drought or pest resistance, for example) into important food crops. Or converting the entire population of a dangerous pathogen into one lacking virulence genes. Or releasing a few mosquitos, allowing them to breed, and creating a population that's incapable of supporting malarial parasite growth. All of these are very real possibilities enabled by the technology.

But there's also a very real risk of a giant, uncontrolled experiment if any of these DNA constructs made it into a wild population. And the developments come at a time where several researchers (including Church) have suggested it's time to lay out some formal guidelines for future research in this area, both for synthetic biology and for human genome modifications. The authors of the fly paper cite two of these editorials, while Science and Nature have run editorials urging that we avoid editing the human germline.

The authors of the fly paper suggest looking to the Asilomar agreement, which was forged by leading biologists who were leaders in the development of recombinant DNA. That created a voluntary yet successful moratorium on the work until safety issues could be examined. We may be forced to see whether this sort of voluntary agreement would hold in an era of intense competition. Similar concerns were voiced about work involving flu viruses, but research continued until the federal government announced a halt to funding for this research.

http://arstechnica.com/science/2014...em-repurposed-to-attack-hiv-where-its-hiding/

As part of its normal life cycle, HIV inserts a copy of itself into the genome of every cell it infects. Most of these copies go on to cause an active infection, pumping out new copies of the virus. A few of them, however, go quiet and can persist even during aggressive antiviral treatments. These infected cells act as a reservoir for the virus, reestablishing an active infection if antiviral therapies are ever stopped. Eliminating this viral reservoir has proven extremely difficult.

Now, researchers are reporting on some of the first tests of a technique that targets the copies of the virus that are lurking in cells with a quiescent infection. Using a system that bacteria utilize to disable viruses, they've shown that it's possible to precisely edit out key HIV DNA sequences, essentially inactivating any copies of the virus. And if placed in cells prior to exposure to HIV, the same system effectively blocks infection.


Bacterial “immune system” used to engineer human DNA in human cells

System lets researchers target changes to specific sites in the genome.
Bacteria don't have an immune system, but that doesn't mean they have no defenses against viruses. When infected, the bacteria can make special RNAs that match the DNA sequences of the virus. These RNAs then guide a protein called Cas9 to the viral DNA, which the protein then cuts. The cut inactivates the virus, protecting the bacteria. The whole system (called CRISPR/Cas) is incredibly flexible; given the right RNA, it can be turned loose on pretty much any DNA sequence. Researchers have shown that it can be used to cut the DNA of living human cells, effectively editing their contents.

That gave a team of biologists an idea. If CRISPR/Cas worked on the DNA of the human genome and HIV inserts itself into said DNA, there's no reason you couldn't target those copies.

So the researchers designed a targeting RNA that would recognize part of the virus that's essential for infection (called an LTR, it controls insertion into the genome and expression of viral genes). They packaged up the genes for that RNA and the Cas9 DNA-cutting protein into a single vector and then inserted the vector into cells that were infected with HIV. As expected, the system cut any copies of HIV that were present in the genome. The cell then typically repaired the DNA by deleting a few nearby bases and relinking the two ends. As a result, key parts of the virus were deleted. The researchers also tested the use of two RNAs that target neighboring sequences and showed that these led to the deletion of all the DNA in between them.

This method was highly efficient, but there were always a few cells left over that seemed to have intact viruses. The researchers don't quite understand why, but it's a safe bet that they're looking into it.

As a further test, the researchers inserted their vector (carrying genes for Cas9 and the targeting RNAs) into the genome of some immune cells. They then attempted to infect those cells with HIV. The vector effectively blocked the establishment of an HIV infection, keeping the cells virus-free; the researchers call these cells "immunized."

It's a promising idea for a potential future therapy, but there are still some roadblocks that need to be dealt with. The first is a lack of complete HIV inactivation—as we mentioned, having any cells left in an HIV-containing reservoir places the patient at risk of having the virus reestablish itself. The second is efficiently getting the vector that contains the CRISPR/Cas system into infected cells. It's rather easy to do in a culture dish, but it's another thing entirely to do it efficiently in the human body. The researchers have their work cut out for them if they want to push this method toward clinical trials.

But even if they don't, using gene editing to block HIV is already in clinical trials. A different technology that makes cuts in DNA is being used to target the gene that encodes one of the proteins that HIV uses to enter cells. We already know that people who lack this gene don't progress to AIDS when infected with HIV, so this approach may not have to work with full efficiency in order to create a population of healthy immune cells in infected patients.

 

[William Gaatjes]

Researchers from the Antoni van Leeuwenhoek hospital in the Netherlands discovered that a certain type of gallbladder cancer is caused by a chronic infection with Salmonella typhi. This cancer is common in countries such as India and Pakistan. The bacteria enters the digestive system and settles under certain conditions inside the gall bladder. Here the bacteria hijacks the cells that line the walls of the gallbladder by releasing specific proteins. These cells can, when infected with another pathogen or because of a genetic predisposition turn into tumor cells.

http://en.wikipedia.org/wiki/Salmonella_enterica_subsp._enterica

Other cancers caused by bacteria is cervical cancer because of an untreated chlamydia infection or Lung cancer because of a chronic mycobacterium tuberculosis infection.

Other cancers in the digestive system may be caused because of other bacteria in the salmonella family. Research is being performed.

 

[tcsenter]

Anecdotal case RE influence of gut bacteria on neurological development or dysfunction:

Father inspired after child's autism improved by course of antibiotic

Father has background in biochemistry/molecular biology. Obvious problem is that it's anecdotal, children with some neurological impairment or developmental delay that could get diagnosed as autistic spectrum often make rapid improvements.

 

[William Gaatjes]

Anecdotal case RE influence of gut bacteria on neurological development or dysfunction:

Father inspired after child's autism improved by course of antibiotic

Father has background in biochemistry/molecular biology. Obvious problem is that it's anecdotal, children with some neurological impairment or developmental delay that could get diagnosed as autistic spectrum often make rapid improvements.

Well, since autism spectrum disorder is such a wide description, different causes may result in similar effect, meaning a diagnosis of autism spectrum disorder. It does not sound unreasonable that when exposed to exotoxins or endotoxins that some neurological effects can be seen. I cannot remember it but there are some bacteria where the toxins produced are neurotoxins. Maybe when being exposed in a constant lower level, neurological changes can happen. But a wrong wiring of neurons can have a similar effect. I will not be surprised that some interesting finds will happen in the future.

 

[William Gaatjes]

About post 279 :
Here we can also read that it is not always one factor that can cause a disease.


http://www.nki.nl/topmenu/about-the...nella-infection-can-cause-gallbladder-cancer/

How a chronic Salmonella infection can cause gallbladder cancer

Cancer is sometimes caused by viruses. A well-known example is that of the virus HPV and cervix cancer. Cancer researchers suspect that bacteria can also sometimes be involved in the development of cancer. But there is little biological evidence for this claim. The research group of prof. dr. Sjaak Neefjes of the Netherlands Cancer Institute has now found such evidence. They show that the bacterium Salmonella Typhi can cause gallbladder cancer. Their results were published on May 28th in the journal Cell Host & Microbe.

Gallbladder cancer is rare in Western countries. But it is quite common in India and Pakistan. Each year around 300.000 people in these two countries are diagnosed with this cancer. There is another disease that if far more common in India and Pakistan than in the West: typhoid fever. This infectious disease is caused by the bacterium Salmonella Typhi. A small percentage of the people who contract this disease will develop a chronic infection, in which the bacteria settles chronically in their gallbladder. This doesn't cause serious symptoms, but these chronically infected people will be able to infect others. And: they appear to be at high risk for developing gallbladder cancer.
Coincidence, or not?

Cancer researchers have therefore suspected for a while that the high incidence of gallbladder cancer in India and Pakistan is linked to the high number of Salmonella infections. But there are other potential risk factors, such as gallstones. In order to take measures against gallbladder cancer in these countries, it is important to establish or exclude Salmonella as a causative agent. The research group of Sjaak Neefjes has now shown that Salmonella infection can indeed transform healthy cells into cancer cells.

An important part of the research was carried out by postdoc researcher Tiziana Scanu. She and Neefjes managed to get hold of gallbladder tumor tissue samples from India and analyzed these. They compared several properties of the gallbladder tumors from India with Dutch gallbladder tumors. One of the things they saw, was that there were distinct genetic differences between the tumors of the two countries. This points to different developmental origins. They also discovered traces of Salmonella Typhi DNA in almost all of the Indian cancer tissues, but none in the Dutch cancer tissues.

Manipulation
These results provided extra proof for a probable causal relationship between Salmonella and gallbladder cancer. Next, Neefjes and Scanu performed several tests with cultured tumor cells, a mouse model and gallbladder tumor organoids. They discovered that Salmonella injects proteins into the gallbladder cells that change certain signaling routes. In a way, the bacterium imposes its will upon the human cell to force the host cell to take up the bacterium and let it grow inside it. Usually, this manipulation process doesn't lead to cancer. But, as Neefjes and Scanu showed, if there are already certain predisposing DNA mutations present in the cell, the manipulation by Salmonella can be the crucial step that transforms the healthy cell into a cancer cell. As a result, cancer is then caused by the fact that Salmonella has to enter cells in its infectious cycle and therefor manipulates various properties of the cell.

This new mechanism for the development of cancer explains why not all people with a chronic Salmonella infection will develop gallbladder cancer. The bacterium contributes to the development of the cancer, but only if there is already a genetic error present within the gallbladder cells. Neefjes suspects that the mechanism he and his team discovered is also used by other bacteria. Neefjes: "There are for instance suspicions of a link between Mycobacterium tuberculosis and lung cancer, and between Chlamydia infection and cervix cancer. These bacteria also manipulate the cells they infect, in the same manner as Salmonella and for the same purpose. So maybe these bacteria also contribute to the development of cancer because of this manipulation process. It would be very interesting to look further into this."

Colon cancer?
But Neefjes himself is for now primarily interested in another issue. Salmonella Typhi isn't common in Western countries, but other types of Salmonella are. Neefjes discovered in his lab that Salmonella Typhimurium, one of the common food poisoning causing bacteria, can contribute to the development of colon cancer in a mouse model. "So, what interests me now, could it be that there is a connection between food poisoning with this type of salmonella and colon cancer in humans?", says Neefjes. "At the moment there is no epidemiological or other type of evidence for this idea, and colon cancer is of course associated with several other risk factors. But maybe Salmonella is one of them. This is what I'd now like to investigate. Because if there is such a link, stricter precautions against Salmonella infection could potentially lower the incidence of colon cancer."

As for the high incidence of gallbladder cancer in India and Pakistan, the present study offers important clues on how to deal with this. Vaccination programs, timely treatment of typhoid fever with antibiotics and sanitary improvements can most probably prevent quite a number of cancer cases is these countries.

 

[William Gaatjes]

When a (soon to be) mother is having a baby, it was always thought that the first contact between bacteria and the baby happens during birth and after birth. But as it turns out, the placenta , an organ that works as an exchange medium between the unborn child and the mother seems not to be sterile.

http://www.nature.com/news/bacteria-found-in-healthy-placentas-1.15274

Bacteria found in healthy placentas
Microbial flora similar to that in the mouth may play a role in preventing preterm births.

The amniotic sac in which a fetus grows is a sterile environment, but the placenta — an organ the fetus shares with the mother — is home to a bacterial community.

The placenta, long thought to be sterile, is home to a bacterial community similar to the one found in the mouth, researchers report today. The microbes are generally non-pathogenic, but according to the authors of the study, variations in their composition could be at the root of common but poorly understood pregnancy disorders such as preterm birth, which occurs in one out of every ten pregnancies.

In 2012, Kjersti Aagaard, an obstetrician at Baylor College of Medicine in Houston, Texas, and her collaborators found that the most abundant microbes in an expectant mother’s vagina were different from those in a non-pregnant woman, but were not generally representative of those that were most common in the stool of an infant in its first week of life1. To investigate where these microbes were coming from, the team decided to examine the placenta.

In the new study, the researchers took samples of placental tissue from 320 women just after delivery, extracted DNA from the tissue and sequenced it. They found that the weight of the mother or whether she gave birth by caesarean or vaginally did not seem to change the makeup of the placental microbiome. But, Aagaard says, the bacterial community “was different among women who either experienced a preterm birth or had a much earlier infection, such as a urinary tract infection — even if that infection was treated and cured many months or weeks previously”. Their findings are published today in Science Translational Medicine2.

The researchers also compared the placental microbiomes to those found in the vagina, gut, mouth and on the skin of non-pregnant women. They found that the placental microbiome was most similar to that of the mouth. The authors speculate that the microbes travel to the placenta from the mouth via the blood. The results reinforce data suggesting a link between periodontal disease in the mother and the risk of preterm birth, says Aagaard.

“This is the first study to show that even in normal pregnancy there is a specific microbiome associated with normal placentation,” says George Saade, an obstetrician at the University of Texas Medical Branch in Galveston, who was not involved in the work.

Roberto Romero, who is program director for perinatal research and obstetrics at the US National Institute of Child Health and Human Development, says that the bacteria the team identified could be from maternal blood rather than being part of a microbial community that lives in the placenta. However Antonio Frias, an obstetrician at Oregon Health & Science University in Portland who was not involved in the study, says the researchers collected the samples ”in a fashion that minimized the risk of potential contamination”.

The team is now studying how women’s microbial communities change during pregnancy. The aim is to identify women at risk of preterm birth, and develop ways to prevent it or deal with its complications in newborns — possibly by using dietary changes to enhance the healthy microbes in the placenta, vagina or the mouth and gut.

 

[William Gaatjes]

Yesterday i watched a documentary and it seems we have to cook our meat thoroughly. That is no news for me, i always eat meat that is prepared well done.
Sometimes meat contaminated with E.Coli 0157 is found and will be recalled.
But before that happens, this little bug can make a person very sick when it gets the change to multiply inside the body.
(Note : In the US).
https://en.wikipedia.org/wiki/Escherichia_coli_O157:H7

EDIT:
That is interesting :

Strains of E. coli that express shiga-like toxins gained this ability due to infection with a prophage containing the structural coding for the toxin, and nonproducing strains may become infected and produce shiga-like toxins after incubation with shiga toxin positive strains. The prophage responsible seems to have infected the strain's ancestors fairly recently, as viral particles have been observed to replicate in the host if it is stressed in some way (e.g. antibiotics).[3][4]
The periplasmic catalase is encoded on the pO157 plasmid, and is believed to be involved in virulence by providing additional oxidative protection when infecting the host.

A prophage is a bacteriophage (often shortened to "phage") genome inserted and integrated into the circular bacterial DNA chromosome or existing as an extrachromosomal plasmid. This is a latent form of a phage, in which the viral genes are present in the bacterium without causing disruption of the bacterial cell.

Another scary one is Salmonella Heidelberg. Scary part about this bacteria is that it is resistant to many antibiotics and makes you sick fast. Someone with a weak immune system can get seriously sick. Yesterday i watched a documentary about a young boy getting a salmonella Heidelberg infection in the brain. Salmonella seems to be a serious problem for the chicken industry.
http://www.cdc.gov/salmonella/heidelberg-10-13/


For those interested :

FRONTLINE
The Trouble with Chicken

FRONTLINE investigates the spread of dangerous pathogens in meat - particularly poultry - and why the food-safety system isn't stopping the threat. Focusing on an outbreak of salmonella Heidelberg at one of the nation's largest poultry processors, the documentary reveals how contaminants are evading regulators and causing more severe illnesses as Americans consume more chicken than ever.

http://video.pbs.org/video/2365487526/

 

[William Gaatjes]

Well, this sure seems promising. An ingredient part of a cancer treatment against skin cancer seems to activate latent hiv viruses hiding inside cells. The problem with current hiv treatment is that viruses hiding in cells do not get killed by the Anti-Retroviral Therapy. These hiding places are called reservoirs. But the ingredient called PEP005 seems to force the hiding viruses out of the reservoirs and makers them vulnerable against ART.

Read it all here in detail :
http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1005066

Abstract :
Although anti-retroviral therapy (ART) is highly effective in suppressing HIV replication, it fails to eradicate the virus from HIV-infected individuals. Stable latent HIV reservoirs are rapidly established early after HIV infection. Therefore, effective strategies for eradication of the HIV reservoirs are urgently needed. We report that ingenol-3-angelate (PEP005), the only active component in a previously FDA approved drug (PICATO) for the topical treatment of precancerous actinic keratosis, can effectively reactivate latent HIV in vitro and ex vivo with relatively low cellular toxicity. Biochemical analysis showed that PEP005 reactivated latent HIV through the induction of the pS643/S676-PKCδ/θ-IκBα/ε-NF-κB signaling pathway. Importantly, PEP005 alone was sufficient to induce expression of fully elongated and processed HIV RNAs in primary CD4+ T cells from HIV infected individuals receiving suppressive ART. Furthermore, PEP005 and the P-TEFb agonist, JQ1, exhibited synergism in reactivation of latent HIV with a combined effect that is 7.5-fold higher than the effect of PEP005 alone. Conversely, PEP005 suppressed HIV infection of primary CD4+ T cells through down-modulation of cell surface expression of HIV co-receptors. This anti-cancer compound is a potential candidate for advancing HIV eradication strategies.

Author Summary

Stable latent viral reservoirs in HIV infected individuals are rapidly reactivated following the interruption of anti-retroviral therapy (ART). Despite an early initiation of ART, viral reservoirs are established and persist as demonstrated in the case of the Mississippi baby and from recent studies of the SIV model of AIDS. Therefore, new strategies are needed for the eradication of the latent HIV reservoirs. We found that ingenol-3-angelate (PEP005), a member of the new class of anti-cancer ingenol compounds, effectively reactivated HIV from latency in primary CD4+ T cells from HIV infected individuals receiving ART. Importantly, a combination of PEP005 and JQ1, a p-TEFb agonist, reactivated HIV from latency at level on average 7.5-fold higher compared to PEP005 alone. The potency of synergistic effects of PEP005 and JQ1 provide novel opportunities for advancing HIV eradication strategies in the future. In summary, ingenols represent a new group of lead compounds for combating HIV latency.

 

[William Gaatjes]

Well, Cancer treatment is improving and i am happy to read about people doing so well. But the earlier it is detected, the better. A blood test would be ideal.
And as it happens, At VUMC it was discovered in 2011 that platelets take in genetic material from tumors. This discovery has led to more research and a trial has been done where a bloodtest was all that is needed to detect tumors.

http://www.vumc.com/

Translated news :
https://translate.google.com/transl...lingen/over-vumc/nieuws/druppel-bloed-kanker/

Researchers at the Cancer Center Amsterdam (CCA) of VU University Medical Center have developed a groundbreaking technique that can detect cancer at an early stage in a drop of blood. Researcher Professor Tom Würdinger of the CCA:.. "It is important to identify cancer as early as possible and treat. The new technique with which we "read" cancer of the blood that play a major role in and hopefully save lives. "It is still in an experimental phase. Würdinger expected within five years to have the test available for the first patients. The discovery is published today by researchers in the prestigious scientific journal Cancer Cell.

Platelets
The research group of Tom Würdinger discovered that platelets of cancer patients RNA (copies of parts of the DNA) contain the tumor. Platelets normally ensure the coagulation of the blood, but recent research shows that platelets also play an important role in tumor growth and metastasis of cancer. The platelets of patients with cancer contain unique RNA-patterns which make it possible to distinguish between healthy individuals of cancer patients with a certainty of 96%.

Better than tissue biopsies and scans
Current detection methods for cancer, such as scans and conventional tissue biopsies, costs a lot of time, are difficult to carry out and expensive. In addition, the decline of tissue in patients taxing, while CT scans to detect only relatively large tumors. The ability to detect tumors in the blood, called 'liquid biopsy', is a major advance for the (early) diagnosis of cancer.

Lots of information in RNA profiles
It turned out to be possible to connect the RNA profile of platelets in cancer patients on the organ in which the tumor has arisen: in the organ in which it was detected, or that it is a metastasis. The platelets profiles can also help to determine what type of therapy is the best. It depends on the mutations in the tumor DNA. It is also possible to see during the treatment of cancer by measurements at different times in the blood or the treatment is effective.

Blood test over five years available
Würdinger: "We are currently working on a fast-usable blood test. This is expected to be available in 2020. The newly developed technique has been tested on the most common tumor types and is widely applicable. In addition, the technique provides an innovative combination of powerful computer algorithms in the diagnosis of cancer through the blood. "

International cooperation
In Amsterdam is currently the CCA Liquid Biopsy Center furnished. The center will collect blood of thousands of cancer patients for further test development and large-scale validation of findings. This happens with different partners. There is a strong cooperation with the US: with Massachusetts General Hospital and Harvard Medical School, and in Europe, for example with the Umea University in Sweden. From VUmc company thromboDx BV has been established that has acquired exclusive rights to the development of these blood tests. It is an app developed that can diagnose via a wifi connection in the future based on the genetic profiles of platelets from patients. For example, able to cooperate hospitals all over the world to the diagnosis and monitoring of cancer.

Read the article online on the website of Cancer Cell
Reference: Best et al, 2015, Cancer Cell 28, 1-11, November 9, 2015, http://dx.doi.org/10.1016/j.ccell.2015.09.018.

And from a newspaper :
The translation from google translate is horrible, but i am too tired to correct it now.

Simple blood test indicates cancer diagnosis within week

Scientists have developed a simple test to cancer with the aid of a few drops of blood can be diagnosed. The international research group led by the Amsterdam hospital VUmc argues that the test within five years on the market.

For the test requires a drop of blood. Of these, the platelets are the smallest blood cells, was examined. The research team discovered in 2011 that platelets genetic material from tumors absorb. Every tumor has other genetic material, also depends on where it is located. By examining the platelets can be determined whether someone has a tumor, what kind and where.

In a test with 283 subjects knew the method in 96 percent of cases, to make an accurate prediction. In addition, the test can discriminate between a primary form of cancer or a metastasis; those predictions were 71 percent of the cases correctly.

Our science editor Margreet Vermeulen phoned Tom Würdinger, the investigator of the project. "Cancer does not deadly disease to be more." (+)

The results were published Thursday in the journal Cancer Cell. Besides scientists from the VU University Medical Center, were also graduates of the AMC, the Radboud University Nijmegen Medical Centre, Harvard Medical School, Massachusetts General Hospital in Boston and the University of Umea in Sweden involved in the research.

In the meantime, there is also carried out a validation study, with seven hundred subjects. From these tests showed the same results. The reliability of the method must be finalized in a US study in which 65 000 women followed for three years.
"No more deadly disease '

This test is much faster than the current procedure, the outcome may be within five to seven days, says research leader and instigator of the American / Swedish / Dutch project Tom Würdinger of VUmc. Moreover, the work is done automatically. This way you save manpower, time and therefore money. The method can be used as the first diagnosis. When the test indicates the presence of a tumor follows a detailed diagnosis.

Professor Würdinger calls the test a breakthrough in the fight against cancer. "If a tumor is detected at a very early stage, existing treatments (chemotherapy, radiation) work much better than it is today. With the result that no cancer deadly disease needs to be more. My dream is that we will in the near future not only every six months, dental checkups, but also let blood test for cancer. "

https://en.wikipedia.org/wiki/Platelet

http://www.cell.com/cancer-cell/abstract/S1535-6108(15)00349-9

PDF of the article :
http://www.cell.com/cancer-cell/pdf/S1535-6108(15)00349-9.pdf

 

[TheVrolok]

Pretty bold statements, I sincerely hope he's right, but I'll still remain quite cautiously optimistic.

 

[William Gaatjes]

I also hope that he is right.

 

[William Gaatjes]

Mycoplasma genitalium is a bacteria that has been identified as a Sexual Transmittable Disease (STD).
It seems that this bacteria can be transmitted through unsafe intercourse.

http://cid.oxfordjournals.org/content/53/suppl_3/S129.full

Abstract

Mycoplasma genitalium is associated with acute and chronic urethritis in men. Existing data on infection in women are limited and inconsistent but suggest that M. genitalium is associated with urethritis, cervicitis, pelvic inflammatory disease, and possibly female infertility. Data are inconclusive regarding the role of M. genitalium in adverse pregnancy outcomes and ectopic pregnancy. Available data suggest that azithromycin is superior to doxycycline in treating M. genitalium infection. However, azithromycin-resistant infections have been reported in 3 continents, and the proportion of azithromycin-resistant M. genitalium infection is unknown. Moxifloxacin is the only drug that currently seems to uniformly eradicate M. genitalium. Detection of M. genitalium is hampered by the absence of a commercially available diagnostic test. Persons with persistent pelvic inflammatory disease or clinically significant persistent urethritis or cervicitis should be tested for M. genitalium, if possible. Infected persons who have not previously received azithromycin should receive that drug. Persons in whom azithromycin therapy fails should be treated with moxifloxicin.

https://en.wikipedia.org/wiki/Mycoplasma_genitalium

Mycoplasma genitalium is a small pathogenic bacterium that lives on the ciliated epithelial cells of the urinary and genital tracts in humans. Its existence was first reported in 1981,[2] and was eventually identified as new species of Mycoplasma in 1983.[1] It can cause significant morbidity in men and women, and is a co-factor in HIV transmission.[3] It is still controversial whether or not these bacterium are to be recognized as a sexually transmitted pathogen, as it is a part of the "natural flora" of many women. Specifically, it causes urethritis (inflammation of the urinary tract) both in men and women, and also cervicitis (inflammation of cervix) and pelvic inflammation in women. Its complete genome sequence was published in 1995.[4] Up until 2003, when a new species of Archaea Nanoarchaeum equitans had its genome sequenced, it was regarded as a cellular unit with the smallest genome.

 

[William Gaatjes]

The researchers in this research, found that they can alter the social behavior
of ants my using epigenetic drugs...

http://www.sciencedaily.com/releases/2016/01/160104080043.htm

date : January 4, 2016
Source: University of Pennsylvania School of Medicine

Social behavior in carpenter ants reprogrammed using epigenetic drugs

Discovery of malleable epigenetic processes in ant brains has implications for
the study of human behavior and disease

In Florida carpenter ant colonies, distinct worker castes called minors and majors exhibit pronounced differences in social behavior throughout their lives. In a new study published today in Science, a multi-institution team anchored at University of Pennsylvania found that these caste-specific behaviors are not set in stone. Rather, this pioneering study shows that social behavior can be reprogrammed, indicating that an individual's epigenetic, not genetic, makeup determines behavior in ant colonies.


Epigenetics is the study of stable, or persistent, changes in gene expression that occur without changes in DNA sequence. Epigenetic regulation has been observed to affect a variety of distinct traits in animals, including body size, aging, and behavior. However, there is an enormous gap in knowledge about the epigenetic mechanisms that regulate social behavior.

Ants provide ideal models to study social behavior, because each colony is composed of thousands of individual sisters -- famously, the queen and all workers are female -- with nearly identical genetic makeup, much like human twins. However, these sisters possess stereotypically distinct physical traits and behaviors based on caste.

In a previous study, the authors created the first genome-wide epigenetic maps in ants. This revealed that epigenetic regulation is key to distinguishing majors as the "brawny" soldiers of carpenter ant colonies, compared to minors, their smaller, "brainier" sisters. Major ants have large heads and powerful mandibles that help to defeat enemies and process and transport large food items. Minor ants are much smaller, outnumber majors two to one, and assume the important responsibility of searching for food and recruiting other ants to help with the harvest. Compared to majors, these foraging minors have genes involved in brain development and neurotransmission that are over expressed.

In the new findings, an interdisciplinary research team led by senior author Shelley Berger, PhD, from the Perelman School of Medicine at the University of Pennsylvania, in collaboration with teams led by Juergen Liebig from Arizona State University and Danny Reinberg from New York University, found that caste-specific foraging behavior can be directly altered, by changing the balance of epigenetic chemicals called acetyl groups attached to histone protein complexes, around which DNA strands are wrapped in a cell nucleus. To reveal this exquisite control, the team demonstrated that foraging behavior could be reprogrammed using compounds that inhibit the addition or removal of these acetyl groups on histones (histone acetylation), in turn changing the expression of nearby genes.

Berger is the Daniel S. Och University Professor in the Departments of Cell & Developmental Biology, Biology, and Genetics. She is also the director of the Penn Epigenetics Program.

"The results suggest that behavioral malleability in ants, and likely other animals, may be regulated in an epigenetic manner via histone modification," said lead author Daniel F. Simola, PhD, a postdoctoral researcher in the Penn Department of Cell and Developmental Biology. Simola is co-lead author with Riley Graham, a doctoral student in the Berger lab.

It's All About the Histone

The almost decade-long collaboration between the Berger, Liebig, and Reinberg labs, supported by the Howard Hughes Medical Institute, blends molecular biology with observations of animal behavior to understand how caste-based differences arise in ants.

Ants, as well as termites, and some bees and wasps, are eusocial (or "truly social") species. Previous work suggested that histone acetylation could create dramatic differences in gene expression between genetically identical individuals, contributing to the physical differences in body size and reproductive ability between ant castes.

The current study expands on this narrative by showing that caste behaviors are also regulated by epigenetic changes in histone acetylation. To do so, the team used the fact that chromatin structure -- the coiling of the DNA around histone proteins -- can be altered by the addition of acetyl groups, which ultimately changes the compaction of the genome. Modifications like histone acetylation allow DNA to uncoil, whereas others cause DNA to become tightly compact and inaccessible to the proteins that regulate gene expression.

Knowing that histone modifications are used to establish specific features of different tissues within an individual led the team to ask whether histone modifications might also be used to create differences in traits like social behavior between individuals, notably the brawny majors and the brainy minors.

In the Science paper, the team fed foraging minors a chemical inhibitor that prevents cells from removing acetyl groups from histones. This treatment enhanced foraging and scouting for food, and correspondingly, led to increased histone acetylation near genes involved in neuronal activity. Conversely, inhibiting the addition of acetyl groups led to decreased foraging activity.

In contrast to the dramatic boost in foraging seen in minors, feeding mature major workers these inhibitors caused little to no increase in foraging. However, the team found that directly injecting these epigenetic inhibitors into the brains of very young majors immediately increased foraging, reaching levels normally only observed in minors. Additionally, a single treatment with these inhibitors was sufficient to induce and sustain minor-like foraging in the majors for up to 50 days. These results suggest that there is an "epigenetic window of vulnerability" in young ant brains, which confers increased susceptibility to environmental manipulations, such as with histone-modifying inhibitors.

Berger observes that all of the genes known to be major epigenetic regulators in mammals are also present in ants, which makes ants "a fantastic model for studying principles of epigenetic modulation of behavior and even longevity, because queens have a much longer lifespan compared to the major and minor workers. Because of the remarkable window we have uncovered, ants also provide an extraordinary opportunity to explore and understand the epigenetic processes that come into play to establish behavioral patterns at a young age. This is a topic of increasing research interest in humans, owing to the growing prevalence of behavioral disorders and diseases and the appreciation that diet may influence behavior."

Broader Implications

One important gene implicated in the ant study is CBP, which is an epigenetic "writer" enzyme that alters chromatin by adding acetyl groups to histones. CBP had already been implicated as a critical enzyme facilitating learning and memory in mice and is mutated in certain human cognitive disorders, notably Rubinstein-Taybi syndrome. Hence, the team's findings suggest that CBP-mediated histone acetylation may also facilitate complex social interactions found in vertebrate species.

The authors suspect that CBP's role as an epigenetic writer enzyme contributes to patterns of histone acetylation that enhance memory pathways related to learned behaviors such as foraging. Differences in CBP activity between minor and major castes may guide unique patterns of gene expression that fine tune neuronal functions for each caste.

"From mammalian studies, it's clear this is an important protein involved in learning and memory," Berger noted. "The finding that CBP plays a key role in establishing distinct social behaviors in ants strongly suggests that the discoveries made in ants may have broad implications for understanding social organization."

The Berger team is now focused on precisely defining the "epigenetic window of vulnerability" and its key molecular features. She explains that "understanding the mechanisms of when and how this window is opened and how changes are sustained -- and why the window closes as the major ant ages -- may have profound implications for explaining human vulnerability to early life exposures."

Story Source:

The above post is reprinted from materials provided by University of Pennsylvania School of Medicine. Note: Materials may be edited for content and length.

 

[William Gaatjes]

Here is a brainfart, either the ADHD and ADD explosion of the last two decades are cooked up ideas by psychologists, or there is an epigenetic factor going on.

 

[William Gaatjes]

I was reading this ars technica article and does make sense. But it may also answer a question :
Many people often asked themselves, why is the birth canal so close to the waste outputs ? Some see it even proof that god does not exist. Either way, nature has its ways to solve biological problems (Which is obvious, duh nature).
But why is it, well, it might be an evolutionary solution to a problem. How to increase the survivability of your child. To give the newborn when born the right bacteria and phages from the mother(besides through the consumption of mother milk).

Here is an idea :
Before a baby is born, the all known fluids break because the amniotic sac tears open. This surely causes some washing of the vagina, flushing out unwanted bacteria and other material.
This could very well clean the vagina a bit but does not make it sterile.
When the baby is pushed from the uterus through the vagina and comes in contact with good bacteria and phages. This helps develop the immune system of the newborn. Also, an epigenetic factor will be in this because the family related bacteria and phages are passed on this way.

For the story read here :

http://arstechnica.com/science/2016...-researchers-smear-babies-with-vaginal-fluid/

It is a small study but it is nevertheless interesting to think about.
When reading it seems icky but when born naturally and not through cesarean delivery this happens anyway.

Birth, like life, is messy. But, while life’s messes often harm health, the untidiness of our entrance into the world may profoundly protect it—at least that’s a leading hypothesis among microbiome researchers.

Microbes picked up from mom while in or exiting the womb kick off humans’ lifelong association with the invisible critters that live in and on us and affect our health. In cases where that microbial colonization of a newborn goes awry, researchers have noted links to chronic health problems, such as asthma, obesity, allergies, and immune deficiencies. Researchers have also found that such a microbial debacle is often brought on by Cesarean delivery (C-section), which is a common surgical procedure to birth a baby through the mother’s abdomen rather than the normal shove down the birth canal.

To reverse the potential ill-fate of C-section babies, researchers smeared surgically delivered babies with the vaginal fluids from their mothers in the moments just after birth. After tracking the babies and their microbiomes for a month, the researchers report Monday in Nature Medicine that the quick slather partly restored normal microbiome development.

The researchers “have taken an important first step toward developing active interventions that may someday enhance the introduction of the newborn to microbial partners and facilitate a lifelong healthy symbiotic relationship,” microbiome researcher Alexander Khoruts of the University of Minnesota, wrote in a commentary on the findings.

For the study, researchers followed 18 babies from birth to one month old. Seven of the babies were born vaginally and 11 were born by C-section. Of those 11 C-section babies, four were rubbed down with vaginal fluids from their mothers. To collect the fluids, researchers placed neatly folded pieces of gauze into the mothers’ vaginas for an hour right before their scheduled C-section. Within the first two minutes after birth, a researcher wiped the microbe-laden gauze over the entirety of the newborn’s body—starting at the lips and smearing to the face, thorax, arms, legs, genitals, anal region, and back.

Then, for the next 30 days, the researcher periodically swabbed the 18 newborns’ mouths, bums, and skin. From the swabs, the researchers analyzed the babies’ microbial communities as they established and evolved.

As in previous data, the researchers noted a clear divergence between the microbial communities on the vaginally delivered babies and those from the un-slathered C-section babies. C-section babies bathed with vaginal fluid, on the other hand, had microbiomes that looked pretty similar to the ones found on the vaginally delivered babies—particularly their skin and oral microbiomes. The anal communities were only partly restored, suggesting their gut microbiomes were still different.

In particular, both vaginally delivered and swabbed C-section babies had early enrichments of Lactobacillus and Bacteroides bacteria, which weren’t seen in unwiped C-section babies.

The data proves that the intervention could alter the babies’ microbiomes. And the researchers are hopeful that further tweaks to the vaginal fluid-smearing could completely mimic the microbial transfer of mother to baby during vaginal delivery.

While promising, the authors cautioned that it’s just an early days proof-of-principle. It’s important to publish this proof-of-principle and make it public now, first author Maria Dominguez-Bello of New York University said, because “it gives credibility,” to the idea. The credibility is sorely needed as she and colleagues compete for grants to do the larger, next-step studies, she said.

Such a long-term study would involve a lot more babies and follow them and their microbiomes for years. The data from such a study could prove that the microbial adjustments from the vaginal swabbing can stick—permanently affecting the microbiome—and, most importantly, improve health.

Nature Medicine, 2015. DOI: 10.1038/nm.4039 (About DOIs).

EDIT:
Since we are under constant attack from good and bad bacteria,.fungi, viruses, worms, parasites and other tiny critters, the birth canal does not need to be a sterile place since we will be under attack as soon as the zygote becomes to exist. The placenta and the amniotic sac will protect the developing child but hey, nature is nature and also the "evil" tiny lifeforms around us are evolving.

 

[William Gaatjes]

With respect to the text in the post above this one (#292) :
I also forgot, That perhaps the high increase of allergies and autoimmune diseases are not caused because the child is to clean as an infant, but perhaps the mother (and father) were to clean prior to the pregnancy and during the pregnancy. Then the baby when born does not get the proper dose of helpful bacteria and phages...
Well, it is just an idea...


EDIT:

I wonder if there ever is a study done with women who practice vaginal douching and newborns with auto immune diseases or allergies or other symptoms that cannot be easily explained...

 

[William Gaatjes]

I recently heard about the bacteria covering our bodies and inside our bodies. As it turns out, it is not that we 100 times as many bacteria living on and inside us but it is more a factor of 3. I tried to look it up, it seems to be in a recent article of nature.

I did not find it, but did found this. Well, it is an old article but nevertheless.
What is interesting is that here also is written that many bacteria can produce chemicals that affect our brains. These chemicals do the same as our neurotransmitters or are just the same neurotransmitters.

What is also written about is a possible link between neurological symptoms and to clean on the maternal side. Very possible that some mental illnesses are indeed caused by a chemical unbalance. But this chemical unbalance is caused by having the wrong bacterial culture inside the intestines from the moment being born. Remember, the immune system of an infant is still developing and being programmed. Maybe, a harmful bacteria could teach the immune system to let it be while being an infant. While the immune system should attack it. This could then turn into a life of misery.
Remember, that the intestines when fully laid out, can cover several thousands of square feet. This to increase the absorption rate. The intestines have a lot of influence on physical and mental well being.

http://www.nature.com/news/gut-brain-link-grabs-neuroscientists-1.16316

Companies selling ‘probiotic’ foods have long claimed that cultivating the right gut bacteria can benefit mental well-being, but neuroscientists have generally been sceptical. Now there is hard evidence linking conditions such as autism and depression to the gut’s microbial residents, known as the microbiome. And neuroscientists are taking notice — not just of the clinical implications but also of what the link could mean for experimental design.

“The field is going to another level of sophistication,” says Sarkis Mazmanian, a microbiologist at the California Institute of Technology in Pasadena. “Hopefully this will shift this image that there’s too much commercial interest and data from too few labs.”

This year, the US National Institute of Mental Health spent more than US$1 million on a new research programme aimed at the microbiome–brain connection. And on 19 November, neuroscientists will present evidence for the link in a symposium at the annual Society for Neuroscience meeting in Washington DC called ‘Gut Microbes and the Brain: Paradigm Shift in Neuroscience’.

Although correlations have been noted between the composition of the gut microbiome and behavioural conditions, especially autism1, neuroscientists are only now starting to understand how gut bacteria may influence the brain. The immune system almost certainly plays a part, Mazmanian says, as does the vagus nerve, which connects the brain to the digestive tract. Bacterial waste products can also influence the brain — for example, at least two types of intestinal bacterium produce the neurotransmitter γ-aminobutyric acid (GABA)2.

The microbiome is likely to have its greatest impact on the brain early in life, says pharmacologist John Cryan at University College Cork in Ireland. In a study to be presented at the neuroscience meeting, his group found that mice born by caesarean section, which hosted different microbes from mice born vaginally, were significantly more anxious and had symptoms of depression. The animals’ inability to pick up their mothers’ vaginal microbes during birth — the first bacteria that they would normally encounter — may cause lifelong changes in mental health, he says.

Similarly, a 2013 study from Mazmanian’s lab found that a mouse model with some features of autism had much lower levels of a common gut bacterium called Bacteroides fragilis than did normal mice3. The animals were also stressed, antisocial and had gastrointestinal symptoms often seen in autism. Feeding B. fragilis to the mice reversed the symptoms. The group also found that the mice with these symptoms had higher levels of a bacterial metabolite called 4-ethylphenylsulphate (4EPS) in their blood, and that injecting that chemical into normal mice caused the same behavioural problems.

The mechanism for these effects is still unclear. At the meeting, Mazmanian will present data showing that feeding 4EPS to mice causes behavioural problems only if the gut is leaky, presumably because that allows the chemical to seep into the body through the intestinal wall. That observation raises the possibility that some people with autism could be supported with therapies, such as probiotics, that target the gut instead of the brain, which is a much more complex and inaccessible organ.

Yet even those at the forefront of the research remain sceptical that the findings will translate into treatments for humans. The evidence that probiotics affect human behaviour “is minimal to say the least”, Mazmanian acknowledges. Still, he says, a growing number of researchers are starting to look at some mental illnesses through a microbial lens.

There are implications for basic research too. In another study to be presented at the meeting, veterinarian Catherine Hagan at the University of Missouri in Columbia compared the gut bacteria in laboratory mice of the same genetic strain that had been bought from different vendors. Their commensals differed widely, she found: mice from the Jackson Laboratory in Bar Harbor, Maine, for instance, had fewer bacterial types in their guts than did mice from Harlan Laboratories, which is headquartered in Indianapolis, Indiana.

Such differences could present a major complication for researchers seeking to reproduce another lab’s behavioural experiments, Hagan says. When her team transplanted bacteria from female Harlan mice into female Jackson mice, the animals became less anxious and had lower levels of stress-related chemicals in their blood. Hagan notes that when a lab makes a mouse by in vitro fertilization, the animal will pick up microbes from its surrogate mother, which might differ greatly from those of its genetic mother. “If we’re going to kill animals for research, we want to make sure they’re modelling what we think they’re modelling,” she says.

 

[William Gaatjes]

One more for the road :

The big question is : Can human gut bacteria alter human behavior as well ?
From previous studies posted in this thread it seems to be that way. But we need more proof. And that will be difficult to get since there will be no human test subjects. It would be devastating if a link is discovered only to find out it is not reversible with current medicine. Imagine a "normal" person in a scientific test turning into a full blown depression sufferer or autism sufferer or add, after being injected with certain bacteria. That would be a really costly problem, making someone sterile again and then re-implanting the proper gut bacteria and hoping that this cures the ailment.

https://www.sciencedaily.com/releases/2015/07/150728110734.htm

Scientists from the Farncombe Family Digestive Health Research Institute at McMaster University have discovered that intestinal bacteria play an important role in inducing anxiety and depression.

The new study, published in Nature Communications, is the first to explore the role of intestinal microbiota in the altered behavior that is a consequence of early life stress.

"We have shown for the first time in an established mouse model of anxiety and depression that bacteria play a crucial role in inducing this abnormal behaviour," said Premysl Bercik, senior author of the paper and an associate professor of medicine with McMaster's Michael G. DeGroote School of Medicine. "But it's not only bacteria, it's the altered bi-directional communication between the stressed host -- mice subjected to early life stress -- and its microbiota, that leads to anxiety and depression."

It has been known for some time that intestinal bacteria can affect behaviour, but much of the previous research has used healthy, normal mice, said Bercik.

In this study, researchers subjected mice to early life stress with a procedure of maternal separation, meaning that from day three to 21, newborn mice were separated for three hours each day from their mothers and then put back with them.

First, Bercik and his team confirmed that conventional mice with complex microbiota, which had been maternally separated, displayed anxiety and depression-like behaviour, with abnormal levels of the stress hormone corticosterone. These mice also showed gut dysfunction based on the release of a major neurotransmitter, acetylcholine.

Then, they repeated the same experiment in germ-free conditions and found that in the absence of bacteria mice which were maternally separated still have altered stress hormone levels and gut dysfunction, but they behaved similar to the control mice, not showing any signs of anxiety or depression.

Next, they found that when the maternally separated germ-free mice are colonized with bacteria from control mice, the bacterial composition and metabolic activity changed within several weeks, and the mice started exhibiting anxiety and depression.

"However, if we transfer the bacteria from stressed mice into non stressed germ-free mice, no abnormalities are observed. This suggests that in this model, both host and microbial factors are required for the development of anxiety and depression-like behavior. Neonatal stress leads to increased stress reactivity and gut dysfunction that changes the gut microbiota which, in turn, alters brain function," said Bercik.

He said that with this new research, "We are starting to explain the complex mechanisms of interaction and dynamics between the gut microbiota and its host. Our data show that relatively minor changes in microbiota profiles or its metabolic activity induced by neonatal stress can have profound effects on host behaviour in adulthood."

Bercik said this is another step in understanding how microbiota can shape host behaviour, and that it may extend the original observations into the field of psychiatric disorders.

"It would be important to determine whether this also applies to humans. For instance, whether we can detect abnormal microbiota profiles or different microbial metabolic activity in patients with primary psychiatric disorders, like anxiety and depression," said Bercik.

 

[William Gaatjes]

Plastics have been and probably always will be a great product. But the problem is pollution and that not all plastics are biodegradable.

But luckily, our little friends are coming to the rescue when it comes to PET :

http://arstechnica.com/science/2016/03/does-newly-discovered-bacteria-recycle-plastic/

Plastics are everywhere. Once they get into the environment as trash, they stay there for years, decades, or even centuries. That's because most plastic is chemically inert and immune to the enzymatic processes involved in biodegradation. We've tried to curtail plastic pollution through recycling and by creating plastics that are biodegradable or compostable. But what about all the plastic litter that's already out there and could persist long after our grandchildren are gone?

Life may be coming to our aid. A team of scientists in Japan, led by Shosuke Yoshida of Kyoto University, has recently discovered a species of bacteria that can degrade a plastic called PET.
Identifying microbes that degrade PET

PET stands for polyethylene terephthalate, a plastic with good mechanical, barrier, and optical properties. Bottles for water and soft drinks are just a couple of PET's many, many uses. PET is a polyester compound with a high aromatic content, which makes it chemically inert. As a result, it is typically considered resistant to microbial degradation, although certain fungi grow on a mineral medium containing PET. Roughly 56 million tons of PET are produced each year, and a lot of that ends up in the environment.

To see whether organisms other than a few fungi can manage to digest this plastic, Dr. Yoshida and his team screened 250 PET debris-contaminated environmental samples. These samples originated in everything from sediment to wastewater. The scientists looked for microorganisms that could use low-crystallinity (1.9 percent) PET film as a major carbon source for growth.

The team identified a distinct microbial consortium that, once cultured, was able to grow on PET. The PET film surface degraded at a rate of 0.13mg per square centimeter each day at 30°C. Under similar conditions, the organisms turned 75 percent of the carbon it obtained from the PET into CO2.

In order to identify the particular organism that was using PET as a carbon source, the scientists diluted the microbial consortium before growing it on PET. The team isolated a novel bacterial species of the genus Ideonella, which they gave the catchy name Ideonella sakaiensis 201-F6. When they discovered a subconsortium that lost the ability to degrade PET, further analysis revealed it lacked I. sakaiensis.

Using the newly identified bacteria, the team almost completely degraded a PET film in just six weeks.
Identifying the enzymes that break down PET

Currently, there are few known enzymes capable of breaking down PET through a chemical process known as hydrolysis. In order to determine what enzymes I. sakaiensis uses, the scientists sequenced its genome. They identified one gene, ISF6_4831 that encodes a protein that shares half of its amino acids with another enzyme that hydrolyzes PET. The area of similarity includes the parts of the enzyme that are used for catalytic activity.

The scientists purified the recombinant protein from I. sakaiensis and incubated it with a PET film at 30°C for 18 hours. The incubation resulted in pitting at the film surface, which is a good indication of degradation. They also performed chemical analysis of the surface, which revealed the presence of certain chemicals including mono(2-hydroxyethyl) terephthalic acid, which is an intermediate for PET hydrolysis.

Using the DNA sequence of the enzyme ISF6_4831, the team built a phylogenetic tree based on enzymes that are known to degrade PET. Using this tree, they identified three other enzymes that they hypothesized could catalyze PET hydrolysis. They then tested their ability to hydrolyze several polymers.

Compared to the three other enzymes, ISF6_4831 had a high preference for PET vs. other polymers with aliphatic esters. As a result, the team called this enzyme “PETase.” They assessed the ability of the PETase to break down the PET found in a typical soda bottle, which has higher crystallinity than their original PET samples—again, it was more active than other enzymes.

While the PETase could break open the PET polymer, it didn't take the polymer all the way to its original starting components, so the team wanted to know whether another enzyme was responsible. Through further gene analysis, the scientists discovered the enzyme ISF6_0224, which has a protein sequence matching those of another enzyme family that is known to hydrolyze the ester linkage of aromatic compounds.

The team purified recombinant ISF6_0224 and found that it was able to efficiently hydrolyze mono(2-hydroxyethyl) terephthalic acid. But when tested against PET, ISF6_0224 did not show any hydrolytic activity. The results strongly suggest that ISF6_0224 protein is responsible for the conversion of mono(2-hydroxyethyl) terephthalic acid (MEHT) into PET’s two environmentally benign monomers, terephthalic acid and ethylene glycol. As such, the team decided that ISF6_0224 should be termed a MEHT hydrolase abbreviated to MEHTase.

This investigation has opened the possibility for a viable remediation strategy for PET. Through further research and development, we could have bacteria that efficiently clean up PET waste.

https://en.wikipedia.org/wiki/Polyethylene_terephthalate


Now we need bacteria that can break down PFOA (C8) into a more harmless substance.
PFOA is all around us in the environment and toxic as well as carcinogenic.


For more information :
http://www.nytimes.com/2016/01/10/magazine/the-lawyer-who-became-duponts-worst-nightmare.html?_r=3

https://en.wikipedia.org/wiki/Perfluorooctanoic_acid

 

[William Gaatjes]

Leids Universitair Medisch Centrum (LUMC) and the TU Delft published an article in Immunity.

The researchers did a mass cytometry on several tissues from the mucus membrane from the intestines of healthy and sick individuals.

https://en.wikipedia.org/wiki/Mass_cytometry

Mass cytometry is a mass spectrometry technique based on inductively coupled plasma mass spectrometry and time of flight mass spectrometry used for the determination of the properties of cells (cytometry).[1][2] In this approach, antibodies are tagged with isotopically pure rare earth elements and these are used to tag the components of cells. Cells are nebulized and sent to an argon plasma, ionizing the multi-atom metal tags, which are then analyzed by a time-of-flight mass spectrometer. The approach overcomes limitations of spectral overlap that limit flow cytometry.

What the researchers found, is that we have more different type of immune cells than expected. That is the idea. From the tissues they researched, 142 different types of immune cells were found.

I am wondering about the idea that we get immune cells as we need them.
Meaning that our immune cells adapt to the specific environment in our body.The bacteria in our large intestine help shape the immune cells.
We have sort of base line cells and cells that adapt to the needed task. If i recall correctly, the same happens for antibodies.
I mean why would epigenetics not be used for to get a specific immune cell up for a given task. Makes sense to me, but it is a guess.



http://www.cell.com/immunity/fulltext/S1074-7613(16)30143-1

Highlights

•Performed high-dimensional analysis of human mucosal immune system by mass cytometry
•Data-driven approaches revealed previously unrecognized immune cell heterogeneity
•Identified mucosal lymphoid malignancies and their cellular precursors
•Data visualizations identified tissue- and disease-associated immune subsets

Summary

Inflammatory intestinal diseases are characterized by abnormal immune responses and affect distinct locations of the gastrointestinal tract. Although the role of several immune subsets in driving intestinal pathology has been studied, a system-wide approach that simultaneously interrogates all major lineages on a single-cell basis is lacking. We used high-dimensional mass cytometry to generate a system-wide view of the human mucosal immune system in health and disease. We distinguished 142 immune subsets and through computational applications found distinct immune subsets in peripheral blood mononuclear cells and intestinal biopsies that distinguished patients from controls. In addition, mucosal lymphoid malignancies were readily detected as well as precursors from which these likely derived. These findings indicate that an integrated high-dimensional analysis of the entire immune system can identify immune subsets associated with the pathogenesis of complex intestinal disorders. This might have implications for diagnostic procedures, immune-monitoring, and treatment of intestinal diseases and mucosal malignancies.

 

[tcsenter]

I was reading this ars technica article and does make sense. But it may also answer a question : Many people often asked themselves, why is the birth canal so close to the waste outputs ?

'A woman can be proud and stiff
When on love intent;
But Love has pitched his mansion in
The place of excrement;
For nothing can be sole or whole
That has not been rent.'

 

[William Gaatjes]

In the US, a person carried a certain bacteria. As it turns out, this bacteria is resistant to colistin. The gene needed for the resistance is carried on a plasmid.
To give a very simple explanation :
If the dna of the bacteria is more like otp(one time programmable) memory, The plasmid is like the ram memory for a bacteria. It can be easily adapted with new data(genes ) and shared easily with other bacteria, even from other bacteria species.


https://www.sciencenews.org/article/bacteria-resistant-last-resort-antibiotic-appears-us?tgt=more

A last-ditch weapon against drug-resistant bacteria has met its match in Pennsylvania.
A 49-year-old woman has tested positive for a strain of Escherichia coli resistant to the antibiotic colistin, researchers report May 26 in Antimicrobial Agents and Chemotherapy.
It’s the first time in the United States that scientists have found bacteria carrying a gene for colistin resistance known as mrc-1, write study coauthor Patrick McGann of Walter Reed Army Institute of Research in Silver Spring, Md., and colleagues.
But perhaps even more alarming is that the gene rides on a transferable loop of DNA called a plasmid.
“That means we now see a possibility of spread,” says physician and clinical microbiologist Robert Skov. And not just from mother cell to daughter cell, he says, but to neighboring strains of bacteria, too.
Bacteria carry most of their genetic information in a tangle of DNA contained in chromosomes inside the cell. But tiny loops of DNA called plasmids hang around outside of the tangle. These loops carry extra information that bacteria can use, like how to protect themselves from antibiotics. Bacteria can swap plasmids like trading cards, effectively spreading instructions for antibiotic resistance.
Countries with antibiotic-resistant mcr-1 gene in humans as of March 1, 2016
GOING GLOBAL An antibiotic-resistant gene, mrc-1, had cropped up in a number of countries across the globe by March 1, 2016. Now, scientists have found E. coli bacteria carrying the gene in the United States, too.
R.L. Skov and D.L. Monnet/Eurosurveillance 2016
In December, Skov and colleagues discovered a Danish patient carrying bacteria with mcr-1 plasmid DNA, like the woman in Pennsylvania. And in November of 2015, researchers reported something similar in China.
Until then, all known colistin resistance was due to tweaks in chromosomal DNA (which, unlike plasmid DNA, isn’t easily spread among bacteria), says Skov, of the Statens Serum Institut in Copenhagen, who was not involved with the new work.
Colistin, a 50-year-old drug that doctors largely stopped prescribing in the 1970s because of its side effects, has made a comeback in the last five to 10 years. It’s used when other antibiotics fail; it’s a treatment option for people infected with multidrug-resistant bacteria. Now, with colistin-resistant bacteria, Skov says, antibiotic treatment options are becoming more and more limited.
The problem, scientists have been pointing out for years, is that people are taking antibiotics too frequently. More use means more opportunity for bacteria to develop resistance.
Still, even with colistin-resistant bacteria emerging all over the world, Skov says he doesn’t expect thousands of people to become infected.
“The scenario now is that once in a while, we’ll see a patient carrying bacteria that we don’t have any good antibiotics left for.” But that, he adds “is dreadful enough.”

More information about plasmids :

http://www.nature.com/scitable/definition/plasmid-plasmids-28

A plasmid is a small, circular, double-stranded DNA molecule that is distinct from a cell's chromosomal DNA. Plasmids naturally exist in bacterial cells, and they also occur in some eukaryotes. Often, the genes carried in plasmids provide bacteria with genetic advantages, such as antibiotic resistance. Plasmids have a wide range of lengths, from roughly one thousand DNA base pairs to hundreds of thousands of base pairs. When a bacterium divides, all of the plasmids contained within the cell are copied such that each daughter cell receives a copy of each plasmid. Bacteria can also transfer plasmids to one another through a process called conjugation.

Scientists have taken advantage of plasmids to use them as tools to clone, transfer, and manipulate genes. Plasmids that are used experimentally for these purposes are called vectors. Researchers can insert DNA fragments or genes into a plasmid vector, creating a so-called recombinant plasmid. This plasmid can be introduced into a bacterium by way of the process called transformation. Then, because bacteria divide rapidly, they can be used as factories to copy DNA fragments in large quantities.

https://en.wikipedia.org/wiki/Plasmid

A plasmid is a small DNA molecule within a cell that is physically separated from a chromosomal DNA and can replicate independently. They are most commonly found in bacteria as small circular, double-stranded DNA molecules; however, plasmids are sometimes present in archaea and eukaryotic organisms. In nature, plasmids often carry genes that may benefit the survival of the organism, for example antibiotic resistance. While the chromosomes are big and contain all the essential information for living, plasmids usually are very small and contain only additional information. Artificial plasmids are widely used as vectors in molecular cloning, serving to drive the replication of recombinant DNA sequences within host organisms.

 

[William Gaatjes]

More links appear between gut bacteria and the brain (at least, in mice but might very well be the case for all mammals).


https://www.sciencenews.org/article/wiping-out-gut-bacteria-impairs-brain?tgt=nr

Obliterating bacteria in the gut may hurt the brain, too.
In mice, a long course of antibiotics that wiped out gut bacteria slowed the birth of new brain cells and impaired memory, scientists write May 19 in Cell Reports. The results reinforce evidence for a powerful connection between bacteria in the gut and the brain (SN: 4/2/16, p. 23).
After seven weeks of drinking water spiked with a cocktail of antibiotics, mice had fewer newborn nerve cells in a part of the hippocampus, a brain structure important for memory. The mice’s ability to remember previously seen objects also suffered.
Further experiments revealed one way bacteria can influence brain cell growth and memory. Injections of immune cells called Ly6Chi monocytes boosted the number of new nerve cells. Themonocytes appear to carry messages from gut to brain, Susanne Wolf of the Max Delbrück Center for Molecular Medicine in Berlin and colleagues found.
Exercise and probiotic treatment with eight types of live bacteria also increased the number of newborn nerve cells and improved memory in mice treated with antibiotics. The results help clarify the toll of prolonged antibiotic treatment, and hint at ways to fight back, the authors write.