[Press release] Among gut microbes, strains, not just species, matter

From the 29 January 2015 University of Washington press release

First large-scale analysis completed of intra-species genetic variation in gut’s resident organisms

By Leila Gray  |  HSNewsBeat  |  Updated 9:00 AM, 01.29.2015

Posted in: Research

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  Gut microbiomes from different people can contain similar microbial species, but different strains, as this cartoon illustrates.Dana C, Thomas

A large community of microorganisms calls the human digestive tract home.  This dynamic conglomerate of microscopic life forms – the gut microbiome – is vital to how people metabolize various nutrients in their food, how their immune systems react to infection, and how they respond to various medications.  Moreover, imbalances in the microbiome are thought to play a significant role in many human diseases.

The collection of species occupying the gut is known to be quite personalized, and people may differ considerably in the set of species they harbor. Now new research suggests that the differences between people may go even deeper. In a paper published Jan. 29 in Cell, researchers at the University of Washington show that even when people share microbes in common, the exact strains each carries might be very different.

“Knowing more about these strain-level variations,” said Elhanan Borenstein, the senior author of this paper and an associate professor of genome sciences at the University of Washington, “is crucial for understanding the complex relationship between the composition of the community of microbes living in the human gut and its influence on health and disease.”

Read the entire article here–http://hsnewsbeat.uw.edu/story/among-gut-microbes-strains-not-just-species-matter

 

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[Press release] Healthy gut microbiota can prevent metabolic syndrome, researchers say

Healthy gut microbiota can prevent metabolic syndrome, researchers say.

From the press release

Posted On November 25, 2014

ATLANTA—Promoting healthy gut microbiota, the bacteria that live in the intestine, can help treat or prevent metabolic syndrome, a combination of risk factors that increases the risk of heart disease, diabetes and stroke, according to researchers at Georgia State University and Cornell University.

Their findings are published in the journal Gastroenterology.

The study, a follow-up to the research team’s previous paper in Science, uses an improved technical approach, making the results more significant.

The research team includes Dr. Andrew Gewirtz, a professor in the Institute for Biomedical Sciences at Georgia State; Dr. Benoit Chassaing, a post-doctoral student at Georgia State; and Dr. Ruth Ley of the departments of Microbiology and Molecular Biology at Cornell.

“These results suggest that developing a means to promote a more healthy microbiota can treat or prevent metabolic disease,” Gewirtz said. “They confirm the concept that altered microbiota can promote low-grade inflammation and metabolic syndrome and advance the underlying mechanism. We showed that the altered bacterial population is more aggressive in infiltrating the host and producing substances, namely flagellin and lipopolysaccharide, that further promote inflammation.”

Metabolic syndrome is a serious health condition that affects 34 percent of American adults, according to the American Heart Association. A person is diagnosed with metabolic syndrome when he or she has three of these risk factors: a large waistline, high triglyceride (type of fat found in the blood) level, low HDL cholesterol level, high blood pressure and high fasting blood sugar. A person with metabolic syndrome is twice as likely to develop heart disease and five times as likely to develop diabetes, according to the National Institutes of Health.

Because metabolic syndrome is becoming more common, scientists are exploring possible causes. In their previous study in Science, Gewirtz, Ley and other researchers showed altered gut microbiota play a role in promoting metabolic syndrome.

Gut microbiota perform key functions in health and when it becomes deregulated it can promote chronic inflammatory diseases such as Crohn’s disease and ulcerative colitis. In addition, altered gut microbiota promote inflammation that leads to metabolic syndrome.

“We’ve filled in a lot of the details about how it works,” Gewirtz said. “It’s the loss of TLR5 on the epithelium, the cells that line the surface of the intestine and their ability to quickly respond to bacteria. That ability goes away and results in a more aggressive bacterial population that gets closer in and produces substances that drive inflammation.”

Normally, the bacteria are in the mucous layer at a certain distance away from epithelial cells. The researchers showed altered gut microbiota is more aggressive in infiltrating the host and gets very close to the epithelium. This altered population produces flagellin and lipopolysaccharide, which further promote inflammation.

The research team improved the study by comparing mice that were siblings and littermates, making all conditions in the study the same. The mice only differed by whether they were missing a specific gene, TLR5. Previously, the researchers studied mice that were from two different strains and lived in separate environments. In this study, they found the absence of TLR5 on the intestinal surface leads to alterations in bacteria that drive inflammation, leading to metabolic syndrome.

This study was funded by the National Institutes of Health and the Crohn’s and Colitis Foundation of America.

[Press release] In the gut, immunity is a 2-way street

From the 10-Jul-2014 EurekAlert

 

The time-course of an immune response begins with the initial pathogen encounter, (or initial vaccination) and leads to the formation and maintenance of active immunological memory. (Photo credit: Wikipedia)

In recent years, it has become increasingly clear that many diseases are triggered or maintained by changes in bacterial communities in the gut. However, the general view up into now has been rather simple: bacteria stimulate the immune system, leading to inflammation or autoimmune disorders in a single direction.

Now, in work published in Immunity, scientists led by Sidonia Fagarasan from the RIKEN Center for Integrative Medical Science in Japan have painted a more complex picture: the gut immune system does not simply prevent the influx of pathogens, but is actively involved in the maintenance of a rich and healthy community of gut bacteria. They propose that faults in the immune regulation lead to changes in the bacterial community that in turn feed back into the immune system.

In the study, the group demonstrated that the regulation by immune T cells of immunoglobulin A (IgA), an antibody that plays a key role in immunity in the gut, is critical for the maintenance of rich bacterial communities in mammal guts.

They began by studying mice with various immune deficiencies and attempted to restore the mice by providing the missing components. They monitored the bacterial communities in the mice’s guts with or without the reconstitutions and evaluated the flow of information between the immune system and bacteria. They discovered that the precise control of IgA production by regulatory T cells is critical for keeping a rich and balanced bacterial community.

To investigate how bacteria feed back to the host, they looked at germ-free mice (mice born and maintained sterile in special incubators) and young pups that had been transplanted with different bacterial communities (either by injection of bacteria or by painting the fur with fecal bacteria extracts from normal or immune-deficient mice). They discovered that the immune system “sees” and responds differently to different bacterial communities. Rich and balanced bacterial communities seem to be perceived as “self” and induce a quick maturation of the immune system and gut responses (induction of regulatory T cells and IgA), while a poor and unbalanced bacterial community is apparently perceived as “non-self” and induces responses aimed at eliminating it (T cells with inflammatory properties and IgG or IgE responses).

According to Sidonia Fagarasan, who led the work, “This study should have an impact on the way we understand immune-related disorders associated with bacteria dysbiosis in the gut. In order to reestablish a healthy state we need to interfere not only with the bacteria, by providing probiotics or through fecal transplantation, but also with the immune system, by correcting the faults caused either by inherited deficiencies or by aging.”

“It was surprising,” she continues, “to see how the reconstitution of T cell-deficient mice with a special regulatory T cell type leads to dramatic changes in gut bacterial communities. It was spectacular to see how the immune system perceives and reacts to different bacteria communities. It gives us hopes that with a better knowledge of the symbiotic relationships between the immune system and bacteria in the gut, we could intervene and induce modifications aiming to reestablish balance and restore health.”

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[Repost] A Galaxy Within Us: Our Gut Microbiota and How It Can Be Programmed by Food

From the1 November 2013 ScienceDaily article

Who would have thought that the human body contains over 10 times the amount of bacterial cells as human cells? These bacteria — now collectively called the gut microbiota — number in their trillions and are made up of more than a 1,000 different species most of which are beneficial in some way.

“Research is starting to show that the food we eat has a huge bearing on the composition of this collective and also that the profile of the collection of bacteria can be associated with a person’s health status,” explains Dr Paul Ross, Head of the Teagasc Food Research Programme and Principal Investigator at the Alimentary Pharmabiotic Centre, Teagasc, Food Research Centre, Moorepark.

To the team at the Alimentary Pharmabiotic Centre (APC), an SFI-funded CSET at Teagasc, Food Research Centre, Moorepark and at University College Cork, the study of the human microbiota has the potential to transform much of the thinking around basic human nutrition, gut health and disease prevention: “This has been made possible through developments made in DNA sequencing technology which has allowed the study of complex microbial communities such as the human gut microbiota, the majority of which cannot be cultured on an individual basis,” explains Dr Ross.

Although the composition of the microbiota is highly stable during adulthood, there are times when it can be highly dynamic — such as at the extremes of life, e.g., following birth, during inflammatory bowel conditions, gastrointestinal infection and in the elderly. Despite this stability, the microbiota also displays a high degree of interindividual variation reflecting differences in lifestyle, diet, host genetics, etc.

In a project called ELDERMET, a team of UCC/Teagasc scientists headed by Professor Paul O’Toole has recently profiled the faecal microbiota from elderly people in different residences including community, day-hospital, rehabilitation or long-term residential care locations.

This study found that the microbiota correlated with the residence location. “The results demonstrated that the individual microbiota of people in long-stay care was significantly less diverse than those that resided in the community,” explains Dr Ross. “In addition, these subjects were also clustered by diet by the same residence location and microbiota groupings. Interestingly, the separation of microbiota composition correlated significantly with health parameters in these individuals including measures of frailty, co-morbidity, nutritional status, markers of inflammation and with metabolites in faecal water.”

Taken together these data suggest that diet can programme the gut microbiota — the composition of which correlates with health status. Such a suggestion opens up great potential for the food industry in the design of food ingredients and supplements which may in the future shape the microbiota in a particular direction to correlate with an improved consumer health status. Interestingly, a related study called INFANTMET, funded by the Department of Agriculture, Food and the Marine and led by Professor Catherine Stanton at Teagasc Moorepark, is looking at the development of the gut microbiota in early life as a consequence of breast feeding.