Abstract

Exposure to psychological stressors can aggravate gastrointestinal inflammatory disorders and enteric infections. Previous work by our lab has shown that mice exposed to a social disruption (SDR) stressor during oral challenge with the colonic pathogen Citrobacter rodentium exhibited increases in colitic pathology, as well as TNF-α and iNOS mRNA levels. Daily treatment with the probiotic bacterium Lactobacillus reuteri ameliorated the heightened inflammation, but the mechanisms by which this occurred are not known. This proposal tested the hypothesis that L. reuteri exerts its beneficial effects by restoring community structure to the commensal gut microbiota. In the first study, germfree mice were colonized with L. reuteri prior to oral challenge with C. rodentium . This monoassociation did not prevent pathogen-induced colitis. Because these mice do not contain commensal microbiota, this indicated that the microbiota are necessary for the protective effects of probiotics to manifest. Thus, a second study was conducted in which the impact of probiotic L. reuteri administration on the commensal gut microbiota was assessed. SDR-exposed mice challenged with C. rodentium had a reduction in commensal genus Lactobacillus . This was abolished in pathogen-challenged mice treated with probiotic Lactobacillus during stressor exposure. Thus, our data indicate that the stressor-induced increases in colitic inflammation during pathogen challenge are associated with shifts to microbiota population abundances and probiotic bacteria ameliorate the inflammatory increases by preventing changes to the gut microbiota.

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