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If taking Clostridia as a probiotic for food allergies works, it would be amazing for food allergy sufferers. Very exciting research. From Time:

The Bacteria That May One Day Cure Food Allergies

Every round of antibiotics a person takes will wipe out strains of bacteria inside the body, some of which are eliminated forever. Considering how early and how often antibiotics are administered to kids—coupled with our increasingly antimicrobial lifestyles—we’ve become more prone to allergies and other ailments, the hygiene hypothesis goes. There’s no cure for food allergies, just lifestyle adjustments and abstention. But Nagler and her team may have the germ of an idea for treatment using gut bacteria, according to a new mice study published in the Proceedings of the National Academy of Sciences.

The team dosed two groups of mice with peanut allergens. One group of mice had been bred to be entirely without gut germs; the other group had sparsely populated gut bacteria due to treatment with antibiotics. Both groups of mice had higher levels of the allergen in their bloodstream compared to mice with healthy gut-bacteria populations.

After giving those same mice a mix that contained the bacteria strain Clostridia, their allergen levels plummeted. Infusing the mice with another group of intestinal bacteria, Bacteroides, didn’t help—so the researchers think the effect is special to Clostridia. “These bacteria are very abundant and they reside very close to the epithelial lining, so they’re in intimate contact with the immune system,” Nagler says.

Next, they’ll transfer gut bacteria from food-allergic infants and healthy infants into germ-free mice, Nagler says. “If we give back Clostridia to a mouse that has the bacteria of an allergic child, can we now reverse susceptibility in that mouse?”

This is a more in-depth article of the research. From Science Daily:

Gut bacteria that protect against food allergies identified

The presence of Clostridia, a common class of gut bacteria, protects against food allergies, a new study in mice finds. The discovery points toward probiotic therapies for this so-far untreatable condition. Food allergies affect 15 million Americans, including one in 13 children, who live with this potentially life-threatening disease that currently has no cure, researchers note.

Although the causes of food allergy -- a sometimes deadly immune response to certain foods -- are unknown, studies have hinted that modern hygienic or dietary practices may play a role by disturbing the body's natural bacterial composition. In recent years, food allergy rates among children have risen sharply -- increasing approximately 50 percent between 1997 and 2011 -- and studies have shown a correlation to antibiotic and antimicrobial use.

"Environmental stimuli such as antibiotic overuse, high fat diets, caesarean birth, removal of common pathogens and even formula feeding have affected the microbiota with which we've co-evolved," said study senior author Cathryn Nagler, PhD, Bunning Food Allergy Professor at the University of Chicago. "Our results suggest this could contribute to the increasing susceptibility to food allergies."

To test how gut bacteria affect food allergies, Nagler and her team investigated the response to food allergens in mice. ...This sensitization to food allergens could be reversed, however, by reintroducing a mix of Clostridia bacteria back into the mice. Reintroduction of another major group of intestinal bacteria, Bacteroides, failed to alleviate sensitization, indicating that Clostridia have a unique, protective role against food allergens.

To identify this protective mechanism, Nagler and her team studied cellular and molecular immune responses to bacteria in the gut. Genetic analysis revealed that Clostridia caused innate immune cells to produce high levels of interleukin-22 (IL-22), a signaling molecule known to decrease the permeability of the intestinal lining.

While complex and largely undetermined factors such as genetics greatly affect whether individuals develop food allergies and how they manifest, the identification of a bacteria-induced barrier-protective response represents a new paradigm for preventing sensitization to food. Clostridia bacteria are common in humans and represent a clear target for potential therapeutics that prevent or treat food allergies. 

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This article summarizes some of the same things I've been posting here. From NY Times:

We Are Our Bacteria

We may think of ourselves as just human, but we’re really a mass of microorganisms housed in a human shell. Every person alive is host to about 100 trillion bacteria cells. They outnumber human cells 10 to one and account for 99.9 percent of the unique genes in the body.

Our collection of microbiota, known as the microbiome, is the human equivalent of an environmental ecosystem. Although the bacteria together weigh a mere three pounds, their composition determines much about how the body functions and, alas, sometimes malfunctions. Like ecosystems the world over, the human microbiome is losing its diversity, to the potential detriment of the health of those it inhabits.

Dr. Martin J. Blaser, a specialist in infectious diseases at the New York University School of Medicine and the director of the Human Microbiome Program, has studied the role of bacteria in disease for more than three decades. In his new book, “Missing Microbes,"Dr. Blaser links the declining variety within the microbiome to our increased susceptibility to serious, often chronic conditions,  from allergies and celiac disease to Type 1 diabetes and obesity. He and others primarily blame antibiotics for the connection.

The damaging effect of antibiotics on microbial diversity starts early, Dr. Blaser said. The average American child is given nearly three courses of antibiotics in the first two years of life, and eight more  during the next eight years. Even a short course of antibiotics like the widely prescribed  Z-pack (azithromycin, taken for five days), can result in long-term shifts in the body’s microbial environment.

But antibiotics are not the only way the balance within us can be disrupted. Cesarean deliveries, which  have soared  in recent decades, encourage the growth of microbes from the mother’s skin, instead of from the birth canal, in the baby’s gut, Dr. Blaser said in an interview.

This change in microbiota can reshape an infant’s metabolism and immune system. A recent review of 15 studies involving 163,796 births found that, compared with  babies delivered vaginally, those born by cesarean section were 26 percent more likely to be overweight and 22 percent more likely to be obese as adults. 

The placenta has a microbiome of its own, researchers have discovered, which may also contribute to the infant’s gut health and help mitigate the microbial losses caused by cesarean sections.

Further evidence of a link to obesity comes from farm animals. About three-fourths of the antibiotics sold in the United States are used  in  livestock. These  antibiotics change the animals’ microbiota, hastening their growth. When mice are given the same  antibiotics used on livestock, the metabolism of their liver changes, stimulating an increase in body fat, Dr. Blaser said.

Even more serious is  the increasing number of serious disorders now linked to a distortion in the microbial balance in the human gut. They include several that are becoming more common in developed countries: gastrointestinal ailments like Crohn’s disease, ulcerative colitis and celiac disease; cardiovascular disease; nonalcoholic fatty liver disease; digestive disorders like chronic reflux; autoimmune diseases like multiple sclerosis and rheumatoid arthritis; and asthma and allergies.

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Even though this study was done in a laboratory, it gives further support for the treatment of sinusitis with bacteria and other microbes. And it could help explain why repeated courses of antibiotics don't "cure"  many chronic infections - because biofilms filled with pathogenic bacteria are signs of microbial communities out-of-whack. Which is why my family's successful chronic sinusitis treatment with kimchi (juice) containing Lactobacillus sakei is all the more impressive. From Science Daily:

Link between antibiotics, bacterial biofilms and chronic infections found

The link between antibiotics and bacterial biofilm formation leading to chronic lung, sinus and ear infections has been found, researchers report. The study results illustrate how bacterial biofilms can actually thrive, rather than decrease, when given low doses of antibiotics. Results of this study may lead to new approach for chronic ear infections in children.

This research addresses the long standing issues surrounding chronic ear infections and why some children experience repeated ear infections even after antibiotic treatment," said Paul Webster, PhD, lead author, senior staff scientist at USC and senior faculty at the Oak Crest Institute of Science. "Once the biofilm forms, it becomes stronger with each treatment of antibiotics."

During the study, non-typeable Haemophilus influenzae (NTHi) bacteria a common pathogen of humans was exposed to non-lethal doses of ampicillin, a class of antibiotics commonly used to treat respiratory, sinus and ear infections, or other beta-lactam antibiotics. The dose of the antibiotic was not enough to kill the bacteria which allowed the bacteria to react to the antibiotic by producing glycogen, a complex sugar often used by bacteria as a food source, to produce stronger biofilms when grown in the laboratory.

Biofilms are highly structured communities of microorganisms that attach to one another and to surfaces. The microorganisms group together and form a slimy, polysaccharide cover. This layer is highly protective for the organisms within it, and when new bacteria are produced they stay within the slimy layer. With the introduction of antibiotic-produced glycogen, the biofilms have an almost endless food source that can be used once antibiotic exposure has ended.

There are currently no approved treatments for biofilm-related infections. Therefore, bacteria forced into forming stronger biofilms will become more difficult to treat and will cause more severe chronic infections. Adults will suffer protracted lung infections as the bacteria hunker down into their protective slime, and children will have repeated ear infections. What may appear to be antibiotic resistance when an infection does not clear up may actually be biofilms at work.

Webster believes modern medicine needs to find ways of detecting and treating biofilm infections before the bacteria are able to form these protective structures. The difficulties of treating biofilm infections, which can be up to 1,000 times more resistant to antibiotics,have prompted some physicians to propose a gradual move away from traditional antibiotic treatments and toward non-antibiotic therapies.

The bacteria called Haemophilus influenzae are a common cause of upper respiratory tract infection. By attaching to surfaces in the body the bacteria form a biofilm. When the bacteria encounter non-lethal amounts of specific antibiotics they are stimulated to form a biofilm, a structure that causes chronic infection and which can be highly resistant to antibiotics. Credit: Paul Webster, Ph.D

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I spent time this past week searching the medical literature (US National Library of Medicine - Medline/PubMed) for the latest in sinusitis research. I wish I could tell you that amazing research has been happening recently, especially with the sinus microbiome (which could mean treating sinusitis with microbes), but I was disappointed. Really disappointed.

I did four searches: one for "sinusitis" (looked at 600+ studies dating back to summer 2013), then "chronic sinusitis" (going back to fall 2012), then "sinusitis, probiotics", and finally "sinusitis, microbiome". The "sinusitis, probiotics" search turned up 10 studies dating back to 2002. The "sinusitis, microbiome" search turned up a grand total of 13 studies, with the oldest dating back to 2004. Of course the sinus microbiome research by Abreu et al from September 2012  discussing Lactobacillus sakei and which I based my personal (and successful) kimchi sinusitis treatment was on the list (see my Dec. 5 post for a discussion of their research). But none of the other studies looked at Lactobacillus sakei (which is in kimchi).

Some of the findings among the many chronic sinusitis studies: microbial diversity is lower in antibiotic treated chronic sinusitis sufferers (than in healthy controls) and the microbial communities more uneven (meaning some microbes dominated over others), and greater Staphylococcus aureus populations among those with chronic sinusitis. After antibiotic treatment patients typically became colonized by microbes that are less susceptible to the prescribed antibiotics. One study found that Staphylococcus epidermidis (SE) may have some effectiveness against Staphylococcus aureus (SA) in the sinusitis microbiome in mice. Lactobacillus rhamnosus was not found to be effective against sinusitis. A number of studies reported biofilms in the sinuses which are highly resistant to medicines. Some studies found that smoking or exposure to second-hand smoke is linked to chronic sinusitis. (June 2016 UPDATE: I should have said that Lactobacillus rhamnosus (R0011 strain) was not effective against sinusitis when taken orally (a tablet) twice a day for 4 weeks in the study. There have been no further studies since then looking at L. rhamnosus for sinusitis treatment. It is unknown whether spraying or smearing/dabbing L. rhamnosus directly into the nostrils would have a positive effect)

Everyone agreed that state of the art genetic analyses found many more microbial species than older methods (the least effective was the traditional culture method). Several studies suggested that perhaps chronic sinusitis is due to immunological defects and one suggested that it was due to "immune hyperresponsiveness" to organisms in the sinuses. Surprisingly, some studies reported that there are more microbes or microbial species in chronic sinusitis patients than in control patients and that Staphylococcus aureus may be dominant (NOTE: These results may be due to not having been done with state of the art genetic analyses which would have picked up more microbial diversity. Another issue is where in the respiratory tract the samples were taken from, because it seems that the different areas have different microbial communities).

There was frequent mention that chronic sinusitis affects millions of people each year in the US, that little is known about its exact cause, and that there is controversy over appropriate treatment. Originally doctors thought that healthy sinuses were sterile, and it has taken a while to realize that is untrue. It is clear that researchers are only now trying to discover what microbial communities live in healthy individuals compared to those with chronic sinusitis.

But it appeared to me that the majority of the studies from the last 2 years indicated that treatment of chronic sinusitis is still: first try antibiotics, then antibiotics plus inhaled corticosteroids and perhaps nasal saline irrigation, then followed by endoscopic sinus surgery (or sometimes balloon dilation), then perhaps steroid drip implants (steroid-eluting sinus implants), and then there may be revision surgeries.

So I'm sticking with my easy-to-do, inexpensive, and fantastically successful kimchi (Lactobacillus sakei) sinusitis treatment. Of course! (see my Dec. 6, 2013 and Feb. 21, 2014 posts or click on the Sinusitis Treatment link for further information).

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Another article stating that the future is feces in treating a number of diseases. From Pacific Standard:

Medicine’s Dirty Secret: Fecal Transplants Are the Next Big Thing in Health Care

POO IS A DECIDEDLY IMPERFECT delivery vehicle for a medical therapy. It’s messy. It stinks. It’s inconsistent, not to mention a regulatory nightmare. But it can be incredibly potent. A classic study of nine healthy British volunteers found that bacteria accounted for more than half of the mass of their fecal solids. That astonishing concentration of microorganisms, both living and dead, makes sense when you consider that the microbial colonists inhabiting our gastrointestinal tract outnumber our own cells roughly three to one, on recent estimates.

In the ideal conditions of the human gut, a thriving ecosystem of 1,000 or more bacterial species that rivals the complexity of a rainforest has co-evolved with us. This microscopic jungle is constantly adapting in response to our diet, antibiotic use and other environmental influences. As the science has progressed, researchers are now comparing the entire collection of microbial inhabitants of the human gut, our microbiome, to a “hidden metabolic organ.” Scientists have linked disruptions to this organ, a condition known as dysbiosis, to everything from inflammatory bowel disease and high blood pressure to diabetes and obesity.

Viewed in this light, a fecal microbiota transplant is nothing more than an attempt to reseed an intestinal tract, often after antibiotics have killed off the native flora that might have kept invasive species at bay. No other medical therapy can claim such a high cure rate for the infection widely known as C. diff.

Some doctors have likened the recoveries of desperately ill patients to those seen with anti-HIV protease inhibitors in the mid-1990s. After the Mayo Clinic in Scottsdale, Arizona, performed its first fecal microbiota transplant in 2011, a patient who had been bed-ridden for weeks left the hospital 24 hours later. And in 2013, researchers in the Netherlands halted a landmark C. diff. clinical trial early for ethical reasons when they saw that the overall cure rate of 94 percent with donor feces had far outpaced the 31 percent cured with the antibiotic vancomycin.

Yet few other interventions elicit such disgust, revulsion, and ridicule. Chronicling a potential advance by a team of Canadian scientists, one newspaper account warned readers: “Hold your nose and don’t spit out your coffee.” In 2013, the founder of a patient advocacy blog called The Power of Poop wrote an open letter to 13 gastroenterology associations detailing the story of a Kentucky man who contracted an acute case of C. diff. Despite his family’s pleas, his doctor dismissed the idea of a fecal transplant as “quackery.” The man died the next day.

Although most providers haven’t published their overall success rates, their self-reported results are surprisingly similar, and consistent with what published reports there are. Khoruts says he has achieved a success rate of about 90 percent after one infusion, 99 percent after two. “In medicine, it’s pretty startling to have therapy that’s that effective for the most refractory patients with that condition,” he says. Colleen Kelly, a gastroenterologist with the Women’s Medicine Collaborative in Providence, Rhode Island, has performed the procedure on 130 patients with recurrent C. diff., with a success rate of about 95 percent. Most of the transplants have taken after just one attempt.

For a relatively simple bacterial infection, Petrof says, the potential remedy may be fairly straightforward. “With recurrent C. diff. what you’ve done is you’ve basically torched the forest,” she says. Nearly everything has been killed off by the antibiotics, leaving very low bacterial diversity. “So the C. diff. can just take root and grow.” Adding back almost any other flora—the equivalent of planting seedlings in the dirt—could help the ecosystem keep interloping pathogens at bay.

For more complicated conditions, though, a simple fecal transplant may not be enough, at least with donors from the Western world. One hypothesis suggests that people in lower-income countries might harbor more diverse bacterial populations in their guts than those who have grown up in a more sterile, antibiotic-rich environment. And in fact, a 2012 study found that residents of Venezuela’s Amazonas state and rural Malawi had markedly more diverse gut microbiomes than people living in three U.S. metropolitan areas. Scientists have already raised the idea that a rise in allergies and autoimmunity in industrialized nations may derive from a kind of collective defect of reduced microbial diversity.

“We cannot find people who’ve never been on antibiotics,” Khoruts says of his donors. For complex autoimmune diseases such as ulcerative colitis, fecal transplants may offer only a partial solution. And with some data suggesting that susceptibility may be linked in part to past antibiotic exposure, perhaps no Western donor can provide the microbes needed to fully reseed the gut.

What then? Khoruts says it may be necessary to seek out ancestral microbial communities—the ones all humans hosted before the advent of the antibiotic era—within people in Africa or the Amazon. “It’s just a disappearing resource,” he says.

By the beginning of April 2014, nearly 30 fecal transplant clinical trials were underway around the world. Roughly half were aimed at C. diff., including two testing the therapy in combination with vancomycin, and another multi-center trial evaluating the effectiveness of fresh versus frozen donor poo.

As the therapy becomes more widely established, via something akin to a “poop pill” or “crapsule,” perhaps the infectious pool of C. diff. patients may start to dwindle. More clinicians, then, might feel emboldened to explore how our bowel flora may affect not only the gastrointestinal system but also the immune and neurological systems. At least a dozen trials are now investigating whether fecal transplants can help treat some form of inflammatory bowel disease, be it Crohn’s disease or ulcerative colitis. Another is looking into Type 2 diabetes, and one is even using lean donors to test fecal transplants on patients with metabolic syndrome. Researchers say it won’t be along before they’re joined by studies investigating whether the therapy might aid diseases like multiple sclerosis and autism.

For those who want to know more, another article form The Pacific Standard:

6 Ways to Transplant Fecal Matter, at Home or at the Hospital

And the following two groups:  The Fecal Transplant Foundation

The Power of Poop

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Excerpts from a very interesting NPR interview with Dr. Martin Blaser and his views on the human microbiome. The big take-away: our modern life-style is not good for the gut microbiome. His recently published book is Missing Microbes: How the Overuse of Antibiotics is Fueling Our Modern Plagues.

From NPR News: Modern Medicine May Not Be Doing Your Microbiome Any Favors

There are lots of theories about why food allergies, asthma, celiac disease and intestinal disorders like Crohn's disease have been on the rise. Dr. Martin Blaser speculates that it may be connected to the overuse of antibiotics, which has resulted in killing off strains of bacteria that typically live in the gut.

Blaser is an expert on the human microbiome, which is the collection of bacteria, viruses, fungi and other microbes that live in and on the body. In fact, up to 90 percent of all the cells in the human body aren't human at all — they're micro-organisms. Blaser is the director of NYU's Human Microbiome Program and a former chairman of medicine there. His new book is called Missing Microbes: How the Overuse of Antibiotics Is Fueling Our Modern Plagues.

"Since World War II, we've seen big rises in a number of diseases: asthma, allergies, food allergies, wheat allergy, juvenile diabetes, obesity. ... These are all diseases that have gone up dramatically in the last 50 or 70 years. One of the questions is: Why are they going up? Are they going up for 10 different reasons, or perhaps there is one reason that is fueling all of them."

"My theory is that the one reason is the changing microbiome; that we evolved a certain stable situation with our microbiome and with the modern advances of modern life, including modern medical practices, we have been disrupting the microbiome. And there's evidence for that, especially early in life, and it's changing how our children develop."

"There's a choreography; there's a normal developmental cycle of the microbiome from birth over the first few years of life, especially the first three years, [that] appear[s] to be the most important. And that's how nature has, how we have, evolved together so that we can maximize health and create a new generation, which is nature's great purpose. And because of modern practices, we have disrupted that. And then the question is: Does that have consequence[s]?"

"As far as we know, when the baby is inside the womb it is apparently sterile. ... The big moment of truth is when the membranes rupture, the water breaks, and the baby starts coming out. And that's where they first get exposed to the bacteria of the world, and the first bacteria they're exposed to is their mother's bacteria in the birth canal. So as labor proceeds, the babies are in contact with the microbes lining their mother's vagina and, as they're going out, they're covered by these bacteria. They swallow the bacteria; it's on their skin. ..."

"That's their initial exposure to the world of bacteria. That's how mammals have been doing it for the last 150 million years, whether they're dolphins or elephants or humans. ... And we know a little about what those bacteria are. The most common bacteria are lactobacillus and there's evidence that over the course of pregnancy the microbiome in the vagina changes, just as many other parts of the body are changing. The microbiome is changing in its composition in terms of maximizing lactobacilli, and these are bacteria that eat lactose, which is the main component of milk. So the baby's mouth is filled with lactobacilli. The first thing that happens is they go up against their mom's breast and they inoculate the nipple with lactobacilli and now milk and lactobacilli go into the new baby and that's the foundation for their microbiome and that's how they start their life. ..."

"You could project that if they didn't acquire these organisms or they didn't acquire them normally or at the normal time, then the foundations might be a little shaky."

"Shortly after birth, they compared the microbiomes in the babies that came out. The babies that were born vaginally, their microbiome, not surprisingly, looked like the mom's vagina everywhere in the body — in their GI tract, on their skin, in their mouth. But the babies born by C-section, their microbiome looked like skin and it didn't even necessarily look like the mom's skin, maybe it was somebody else in the operating room. So it's clear that the microbiome is different immediately depending on the kind of birth."

"What I can tell you is that our immune system is quite complex. There are many kinds of immune cells. There are cells that strongly recognize foreign substances, there are ones that try to damp [the immune system] and down-regulate it. There's what we call innate immunity, which is the immunity we're all born with, and then there's adaptive immunity — the immunity that develops when we experience different kinds of exposures. So it's very complex."

"There are many different probiotics.  I think I can say three things: The first is that they're almost completely unregulated; second is that they seem to be generally safe; and third is that they're mostly untested. ... I'm actually a big believer in probiotics; I think that's going to be part of the future of medicine, that we're going to understand the science of the microbiome well enough so that we can look at a sample from a child and say this child is lacking such-and-such an organism and now we're going to take it off the shelf and we're going to give it back to that child. ... "

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Another article reporting on the Crohn's disease study I posted yesterday. But this article lists the depleted bacteria and also which ones there are too much of in Crohn's patients. It illustrates that gut microbial communities being out of whack go hand in hand with disease. Remember: dysbiosis means an imbalance in the microbial populations. Interestingly, just like in the 2012 sinusitis study (see my December 4, 2013 post) - it's biopsies that found the specific bacterial imbalances, and not fecal samples or mucus/phlegm swabs (typically done in sinusitis). Big step forward in human microbiome research. And again antibiotics are not the answer.

From Science magazine:

Crohn's Disease Marked by Dramatic Changes in Gut Bacteria

The largest clinical study of its kind is revealing new insights into the causes of Crohn's disease, a periodic inflammation of the intestines. The research, which involved 668 children, shows that numbers of some beneficial bacteria in the gut decrease in Crohn's patients, while the number of potentially harmful bacteria increases. The study could lead to new, less invasive diagnostic tests; it also shows that antibiotics—which aren't recommended for Crohn's but are often given when patients first present with symptoms—may actually make the disease worse.

Crohn’s disease is one of the two major inflammatory bowel diseases (IBDs); the other is ulcerative colitis, a similar condition that affects only the colon. Both have been on the rise in the developing world since the early 1950s; now, an estimated 1.4 million people suffer from IBD in the United States alone. Symptoms include diarrhea, abdominal pains and cramping, and intestinal ulcers.

But genes alone can't explain the sharp rise in IBD incidence, and scientists have looked at the environment—in particular diet and antibiotic use—for answers.

Several studies have shown that Crohn’s disease is characterized by microbial dysbiosis, a shift in the microbial populations inhabiting the gut, but it's difficult to unravel cause and effect: A change in gut microbiota can cause inflammation, but the reverse can also occur. Complicating the picture is the fact that before being diagnosed with IBD, patients often receive antibiotics to fend off a supposed gut infection that could be causing the symptoms, which also have a powerful impact on the microbial populations living in our guts.

Now, a group headed by Ramnik Xavier, a gastroenterologist at Harvard Medical School in Boston, has collected fecal samples and taken biopsies of the lower part of the small intestine and rectum from 447 children who had just been diagnosed with Crohn's, and a control group of 221 kids who had noninflammatory abdominal symptoms, such as bloating and diarrhea. In contrast with previous studies, the majority of patients had not yet received antibiotics or anti-inflammatory drugs. Based on their genetic material, the researchers determined the relative abundance of a range of microbial species in the samples.

Some potentially harmful microbial species were more abundant in Crohn's patients, such as those belonging to the Enterobacteriaceae, Pasteurellaceae, Veillonellaceae, and Fusobacteriaceae; numbers of the Erysipelotrichales, Bacteroidales, and Clostridiales, generally considered to be beneficial, were lower. The disappearance and appearance of species can be equally important, says Dirk Gevers of the Broad Institute in Cambridge, Massachusetts, who performed most of the work. "There has been a shift in the ecosystem, which affects both types.”

But those differences were found mostly in the biopsy samples; there weren't many differences between the feces from Crohn's patients and the control group. At this early stage of the disease, "the dysbiosis seems not to have reached the stool yet," Gevers says.

The dysbiosis was also more pronounced in patients who had received antibiotics. "This study confirms that these drugs don’t do any good to people with Crohn’s disease," says gastroenterologist Séverine Vermeire of the Catholic University of Leuven in Belgium, who was not involved in the study. "We knew antibiotic use increases the risk to develop the disease; now we know they can worsen it, too."

Vermeire says it's a "missed opportunity" that the researchers didn't look at the patients' diets. "That could have helped elucidate why this disease occurs so much more in the Western world than elsewhere." In 2011, Vermeire’s group published a study showing that healthy family members of Crohn's disease patients have a slight dysbiosis as well. Vermeire is convinced that even in these families, it's not genetics but some lifestyle factor that causes the phenomenon. "If we could identify the dysbiosis in an early stage, and we knew the causative factors,” she says, “we could prevent disease occurrence by bringing about lifestyle changes.”

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Two related studies showing the importance of the intestinal bacterial community for health and preventing diseases. Both also discuss how antibiotics disrupt the gut microbial community. From Science Daily:

Microbes help to battle infection: Gut microbes help develop immune cells, study finds

The human relationship with microbial life is complicated. Although there are types of bacteria that can make us sick, Caltech professor of biology and biological engineering Sarkis Mazmanian and his team are most interested in the thousands of other bacteria -- many already living inside our bodies -- that actually keep us healthy. Now, he and his team have found that these good bugs might also prepare the immune cells in our blood to fight infections from harmful bacteria.

In the recent study, published on March 12 in the journal Cell Host & Microbe, the researchers found that beneficial gut bacteria were necessary for the development of innate immune cells -- specialized types of white blood cells that serve as the body's first line of defense against invading pathogens.

In addition to circulating in the blood, reserve stores of immune cells are also kept in the spleen and in the bone marrow. When the researchers looked at the immune cell populations in these areas in so-called germ-free mice, born without gut bacteria, and in healthy mice with a normal population of microbes in the gut, they found that germ-free mice had fewer immune cells -- specifically macrophages, monocytes, and neutrophils -- than healthy mice. Germ-free mice also had fewer granulocyte and monocyte progenitor cells, stemlike cells that can eventually differentiate into a few types of mature immune cells. 

Khosravi and his colleagues next wanted to see if the reduction in immune cells in the blood would make the germ-free mice less able to fight off an infection by the harmful bacterium Listeria monocytogenes -- a well-studied human pathogen often used to study immune responses in mice. While the healthy mice were able to bounce back after being injected with Listeria, the infection was fatal to germ-free mice. When gut microbes that would normally be present were introduced into germ-free mice, the immune cell population increased and the mice were able to survive the Listeria infection.

The researchers also gave injections of Listeria to healthy mice after those mice were dosed with broad-spectrum antibiotics that killed off both harmful and beneficial bacteria. Interestingly, these mice also had trouble fighting the Listeria infection. "We didn't look at clinical data in this study, but we hypothesize that this might also happen in the clinic," says Mazmanian. "For example, when patients are put on antibiotics for something like hip surgery, are you damaging their gut microbe population and making them more susceptible to an infection that had nothing to do with their hip surgery?"

More importantly, the research also suggests that a healthy population of gut microbes can actually provide a preventative alternative to antibiotics, Khosravi says. 

From Science Daily:

Large study identifies exact gut bacteria involved in Crohn's disease

While the causes of Crohn's disease are not well understood, recent research indicates an important role for an abnormal immune response to the microbes that live in the gut. In the largest study of its kind, researchers have now identified specific bacteria that are abnormally increased or decreased when Crohn's disease develops. The findings, which appear in the March 12 issue of the Cell Press journal Cell Host & Microbe, suggest which microbial metabolites could be targeted to treat patients with this chronic and currently incurable inflammatory bowel disease.

Twenty-eight gastroenterology centers across North America have been working together to uncover how microbes contribute to the inflammatory cascade of Crohn's disease. Researchers took biopsies from 447 individuals with new-onset Crohn's disease and 221 nonaffected individuals at multiple locations along the gastrointestinal tract and then looked for differences between the two groups. They also validated their methods in additional individuals, resulting in a total of 1,742 samples from pediatric and adult patients with either new-onset or established disease.

The team found that microbial balance was disrupted in patients with Crohn's disease, with beneficial microbes missing and pathological ones flourishing. Having more of the disease-associated organisms correlated with increasing clinical disease activity. 

When the researchers analyzed the effects of antibiotics, which are sometimes used to treat Crohn's disease symptoms prior to diagnosis, they found that antibiotic usage in children with Crohn's disease could be counterproductive because it causes a loss of good microbes and an increase in pathological ones.

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Some recent studies have explored the link between bacteria in the gut and colorectal cancer. The beneficial Prevotellaceae bacteria (mentioned in the Nov. 5 study below) have been discussed elsewhere as liking whole grain foods. So go feed your gut with some nice whole grain bread or cereal. And some fruits and veggies while you're at it. As mom used to say: "You are what you eat."

A study published December 6, 2013 found that decreased diversity of the gut microbiome and the presence of certain types of bacteria were associated with colorectal cancer in humans: Decreased Diversity of Bacteria Microbiome in Gut Associated Colorectal Cancer

From the November 5, 2013 Science Daily: Microbes in the Gut Help Determine Risk of Tumors

Transferring the gut microbes from a mouse with colon tumors to germ-free mice makes those mice prone to getting tumors as well, according to the results of a study published in mBio®, the online open-access journal of the American Society for Microbiology. The work has implications for human health because it indicates the risk of colorectal cancer may well have a microbial component.

Scientists have known for years that inflammation plays a role in the development of colorectal cancer, but this new information indicates that interactions between inflammation and subsequent changes in the gut microbiota create the conditions that result in colon tumors.

Known risk factors for developing colorectal cancer include consuming a diet rich in red meat, alcohol consumption, and chronic inflammation in the gastrointestinal tract (patients with inflammatory bowel diseases, such as ulcerative colitis, are at a greater risk of developing colorectal cancer, for instance).

The results were stark: mice given the microbiota of the tumor-bearing mice had more than two times as many colon tumors as the mice given a healthy microbiota. What's more, normal mice that were given antibiotics before and after inoculation had significantly fewer tumors than the mice that got no antibiotics, and tumors that were present in these antibiotic-treated mice were significantly smaller than tumors in untreated mice. This suggests that specific populations of microorganisms were essential for the formation of tumors...

Looking at the microorganisms, they found that tumor-bearing mice harbored greater numbers of bacteria within the Bacteroides, Odoribacter, and Akkermansia genera, and decreased numbers of bacteria affiliated with members of the Prevotellaceae and Porphyromonadaceae families. Three weeks after they were inoculated with the communities from the tumor-bearing mice, the germ-free mice had a gut microbiome that was very similar to the tumor-bearing mice, and they had a greater abundance of the same bacterial groups associated with tumor-formation. 

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There is a new procedure in which microbiota (the microbes) from a healthy individual are introduced into the gastrointestinal system of a diseased individual via a fecal transplant.  The purpose of the fecal transplant is to replace good bacteria which has been suppressed or killed (usually by antibiotics) , and which has caused bad bacteria, such as Clostridium difficile, to overpopulate the gut. This is having amazing success rates.  It has been used the most for Clostridium difficile (C. difficile) infections, which sickens about half a million Americans annually. This infection can be so debilitating and so resistant to all antibiotics that about 14,000 Americans die each year from it. Even though not that many have been done, fecal transplants are gaining in popularity (some even being done by do-it-yourselfers using fecal enemas at home) because fecal transplants can have a 95 to 98% success rate.                      

New research is starting to see if the fecal transplant can be made even easier (via a "poop pill"), and also if fecal transplants will work for Inflammatory Bowel Diseases (IBD). This would mean the future treatment possibility of transplanting microbiota from healthy individuals to individuals sick with IBD. From the October 4, 2013 Science Daily:  

 Fecal Transplant Pill Knocks out Recurrent C. Diff Infection

C. diff infection can occur after people take antibiotics, wiping out the good bacteria in the gastrointestinal (GI) system, allowing C. diff to flourish and leading to severe diarrhea. In some patients, infection continues to recur despite standard treatment with antibiotics. For patients trapped in that cycle, doctors have transplanted feces from healthy donors into their GI system to rebalance the bacteria and stop infections from recurring.

University of Calgary researchers reported a 100 percent success rate -- none of the 27 patients who took the tablet-sized pills had a recurrence of C. diff, even though all of them previously had had at least four bouts of the infection. Patients ingested between 24 and 34 capsules containing fecal bacteria, often donated by family members.

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There is even the site The Power of Poop  which calls itself a "patient information resource dedicated to promoting safe accessible Fecal Microbiota Transplant (FMT) and to raising awareness of the role of the human microbiome in digestive illness."    http://thepowerofpoop.com