JULY 2008


Bacterial by-product wards off colitis

When sugar molecule missing, along comes IBD. The gut demystified

Bacteroides fragilis, a common boarder in the human gut, may play a role in preventing colitis

Rather than being passive guests in the gut, certain bacteria appear to play a crucial role in the prevention of diseases such as colitis, new research in the May 29 issue of Nature suggests. Scientists hope that this finding will help develop new approaches to treating inflammatory bowel disease (IBD).

Zeroing in on the microbe Bacteroides fragilis, a common boarder in the human gut, the researchers discovered that this bacterium excretes a sugar molecule that tampers with the immune system of its host. When the organism was missing in the gut microflora of mice bred to develop colitis, the rodents came down with severe symptoms of the disease. But they were virtually disease-free when the microbes were present.

"This is the first proof that an imbalance in normal gut bacteria can cause colitis," study author Dr Dennis Kasper, a physician microbiologist at Harvard Medical School, told NRM. Until now, researchers had assumed that the microbe in question did neither harm nor good, but it turns out that B fragilis is a real team player. The bacterium produces a sugar molecule, polysaccharide A (PSA), that stimulates the release of anti-inflammatory cytokines in the host's bowel. It also suppresses the release of pro-inflammatory substances in the gut.

To check whether PSA really was what was protecting the colitis-prone mice from disease, the researchers purified the substance and fed it dir-ectly to the animals. What followed was a bit of a eureka moment. "If you give them pure PSA, they don't get col-itis," beams Dr Kasper. This is huge because it pinpoints exactly how the bacteria interact with a host's immune system. The idea of beneficial bacteria isn't new, but until now, the mechanism wasn't clear: "In Europe they sell probiotics by the gallon, and it's never been shown scientifically how it's supposed to work," Dr Kasper says.

Establishing the link between microbe and mammal may point the way to developing new approaches to treating IBD. The authors write that "symbiosis factors such as PSA might potentially provide therapeutics for human inflammatory disorders on the basis of entirely novel biological principles." And there may be many more — as yet unknown — associations between bacteria and their hosts. For example, imbalances in the gut microcosmos might also help explain other diseases, including food allergies and asthma. To date, we know very little about the microbes that dwell in our intestines: "There are trillions of bacteria in the human gut, and we can't even grow most of them," Dr Kasper says.

While B fragilis is common in the human bowel, the etiology of colitis in people may differ from that in mice. For instance, the researchers used the bacterium Helicobacter hepaticus to induce colitis in the rodents, but this organism isn't known to have the same effect in the human gut. Truth is, the causes of IBD in people aren't well understood at all. The condition is attributed to an aberrant immune response directed at normal everyday bacteria in the gut that usual-ly do no harm. No one's sure why these bacteria are being targeted.

One popular theory is the 'hygiene hypothesis,' the idea that a lack of exposure to both pathogenic and symbiotic microbes in early childhood adversely affects maturation of the immune system. The Nature study supports this hypothesis as it shows that disease — in this case colitis — may result from the absence of beneficial gut bacteria and the molecules they produce.



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