Gut feeling: Researchers find bacteria that relieve IBD symptoms in mice

A team of academic researchers have found a single bacterial molecule that can relieve symptoms in a mouse model of inflammatory bowel disease (IBD), paving the way for development of natural remedies for inflammatory disorders in humans.

Amy Swinderman
PASADENA, Calif.—A team of academic researchers have found a single bacterial molecule that can relieve symptoms in a mouse model of inflammatory bowel disease (IBD), paving the way for development of natural remedies for inflammatory disorders in humans.

According to findings recently published in the science journal Nature, the researchers found a typical stomach bacterial strain protects against an inflammatory disease similar to inflammatory bowel disease in mice. The study was co-authored by Dr. Dennis Kasper of Harvard Medical School, Dr. Sarkis Mazmanian of the California Institute of Technology and Marika Kullberg of the Hull York Medical School in England.

"IBD is strongly believed to be an aberrant and uncontrolled immune response directed toward intestinal bacteria," Mazmanian says. "The resulting inflammation causes damage to the gut, resulting in the pathology observed in patients with Crohn's disease and ulcerative colitis. We wanted to know if symbiotic beneficial bacteria of the mammalian gastrointestinal tract can provide protection from experimental colitis in animal models of disease."

According to the researchers, a stomach bacterial strain, Bacteroides fragilis, protects against an inflammatory disease similar to IBD in mice caused by another typical stomach bacterium, Helicobacter hepaticus, with pathogenic potential. The team identified a single molecule produced by B. fragilis, polysaccharide A (PSA), which is responsible for preventing disease.

"In animals harboring B. fragilis not expressing PSA, H. hepaticus colonization leads to disease and pro-inflammatory cytokine production in colonic tissues," the researchers wrote. "Purified PSA administered to animals is required to suppress pro-inflammatory interleukin-17 production by intestinal immune cells and also inhibits in vitro reactions in cell cultures. Furthermore, PSA protects from inflammatory disease through a functional requirement for interleukin-10-producing CD4+ T cells."

These results show that molecules of the bacterial microbiota can mediate the critical balance between health and disease, the researchers wrote.

"Harnessing the immunomodulatory capacity of symbiosis factors such as PSA might potentially provide therapeutics for human inflammatory disorders on the basis of entirely novel biological principles," the researchers predict.

"The next step is to understand what are the cellular and molecular requirements for the immune responses to PSA," Mazmanian says. "Thus, what cell types are affected during protection from disease, and how do these changes to the cell control gut pathology. It is very difficult to speculate the long-term impact of these findings, as our understanding of the precise mechanisms of this discovery are still in their infancy. However, one can imagine someday treating those at high-risk for IBD with bacterial molecules as therapies. This notion would require a significant amount of additional experimental information."

Amy Swinderman

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