Modulation of host immune responses by the cytolethal distending toxin of Helicobacter hepaticus.

Persistent murine infection with Helicobacter hepaticus leads to chronic gastrointestinal inflammation and neoplasia in susceptible strains. To determine the role of the virulence factor cytolethal distending toxin (CDT) in the pathogenesis of this organism, interleukin-10-deficient (IL-10-/-) mice were experimentally infected with wild-type H. hepaticus and a CDT-deficient isogenic mutant.

Colonization of the cecal mucosa by Helicobacter hepaticus impacts the diversity of the indigenous microbiota.

Establishment of mucosal and/or luminal colonization is the first step in the pathogenesis of many gastrointestinal bacterial pathogens. The pathogen must be able to establish itself in the face of competition from the complex microbial community that is already in place. We used culture-independent methods to monitor the colonization of the cecal mucosa of Helicobacter-free mice following experimental infection with the pathogen Helicobacter hepaticus.