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Background  The zoonotic pathogen  Campylobacter jejuni  is a leading cause of bacterial foodborne enterocolitis in humans worldwide. The understanding of immunopathology underlying human campylobacteriosis is hampered by the fact that mice display strong colonization resistance against the pathogen due to their host specific gut microbiota composition.    Methodology/Principal Findings  Since the microbiota composition changes significantly during intestinal inflammation we dissected factors contributing to colonization resistance against  C. jejuni  in murine ileitis, colitis and in infant mice. In contrast to healthy animals  C. jejuni  could stably colonize mice suffering from intestinal inflammation. Strikingly, in mice with  Toxoplasma gondii -induced acute ileitis,  C. jejuni  disseminated to mesenteric lymphnodes, spleen, liver, kidney, and blood. In infant mice  C. jejuni  infection induced enterocolitis. Mice suffering from intestinal inflammation and  C. jejuni  susceptible infant mice displayed characteristical microbiota shifts dominated by increased numbers of commensal  Escherichia coli . To further dissect the pivotal role of those distinct microbiota shifts in abrogating colonization resistance, we investigated  C. jejuni  infection in healthy adult mice in which the microbiota was artificially modified by feeding live commensal  E. coli . Strikingly, in animals harboring supra-physiological intestinal  E. coli  loads, colonization resistance was significantly diminished and  C. jejuni  infection induced enterocolitis mimicking key features of human campylobacteriosis.    Conclusion/Significance  Murine colonization resistance against  C. jejuni  is abrogated by changes in the microbiota composition towards elevated  E. coli  loads during intestinal inflammation as well as in infant mice. Intestinal inflammation and microbiota shifts thus represent potential risk factors for  C. jejuni  infection. Corresponding interplays between  C. jejuni  and microbiota might occur in human campylobacteriosis. Murine models introduced here mimick key features of human campylobacteriosis and allow for further analysis of immunological and molecular mechanisms of  C. jejuni  – host interactions.

Intestinal Microbiota Shifts towards Elevated Commensal Escherichia coli Loads Abrogate Colonization Resistance against Campylobacter jejuni in Mice