The mediator of interest is the regulatory T (Treg) cell population, which suppresses inflammation and is depleted in germ-free mice that lack commensal bacteria. Having previously observed a boost in the number of Treg cells in the colon of germ-free mice after these mice ingested chloroform-resistant, spore-forming bacteria from normal mouse feces, the team searched for similar Treg-boosting bacteria in the human gut microbiota2. Sure enough, ingestion of the chloroform-resistant fraction of human feces induced the appearance of Treg cells in the colon of germ-free mice. To identify the particular bacterial strains driving Treg development, Honda and co-workers cloned over 400 bacterial colonies from the guts of these mice. Genomic analysis revealed that all clones were members of the genus Clostridium and none encoded strong virulence-related genes. A mixture of only 17 of these clostridia strains was sufficient to recapitulate the Treg cell–promoting effect of the entire chloroform-resistant feces fraction and to reduce the severity of experimentally induced allergic diarrhea and colitis. This effect was robust, as it was observed in mice of different genetic backgrounds and in rats.
Fredrik Bäckhed at the University of Gothenburg, Sweden, concludes that “this is a really important study because the field is a little bit stuck, in that most mechanistic studies are done in mice, and most correlative studies are done in humans. This particular study is a step forward because it represents an intermediate between mouse and man.”
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