Gut flora generally contributes to a healthy environment while both commensal and pathogenic bacteria that influence the innate and adaptive immune responses, can cause acute and/or chronic mucosal inflammation. Citrobacter rodentium (C. rodentium) is a member of the family of enteropathogens that provide an excellent in vivo model to investigate the host-pathogen interactions in real-time. It is the etiologic agent for transmissible murine colonic hyperplasia (TMCH) while inflammation following C. rodentium infection is dependent upon the genetic background. Ongoing and completed studies in this model have so far established that Wnt/β-catenin, Notch and PI3K pathways regulate colonic crypt hyperplasia while epithelial-stromal cross-talk, mediated by MEK/ERK/NF-κB signaling, regulates inflammation and/or colitis in susceptible strains. The C. rodentium-induced hyperplastic state also increases the susceptibility to either mutagenic insult or in mice heterozygous for Apc gene. The ability to modulate the host response to C. rodentium infection therefore provides an opportunity to delineate the mechanisms that determine mucosal hyperplasia, intestinal inflammation, and/or neoplasia as disease outcomes.
Keywords: Citrobacter rodentium; Colon Cancer; Enteric Infection; Inflammation; Inflammatory Bowel Disease; Microbiota; Wnt Signaling.