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Colonization parameters, pathology, serology, and inflammatory responses to wild-type<jats:italic>H. cinaedi<\/jats:italic>(WT<jats:sub>Hc<\/jats:sub>) were evaluated in B6.129P2-<jats:italic>IL-10<\/jats:italic><jats:sup><jats:italic>tm1Cgn<\/jats:italic><\/jats:sup>(IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>) mice for 36 weeks postinfection (WPI) and in C57BL\/6 (B6) mice for 12 WPI. Because cytolethal distending toxin (CDT) may be a virulence factor, IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>mice were also infected with the<jats:italic>cdtB<\/jats:italic><jats:sub>Hc<\/jats:sub>and<jats:italic>cdtB<\/jats:italic>-N<jats:sub>Hc<\/jats:sub>isogenic mutants and evaluated for 12 WPI. Consistent with other murine enterohepatic helicobacters, WT<jats:sub>Hc<\/jats:sub>did not cause typhlocolitis in B6 mice, but mild to severe lesions developed at the cecocolic junction in IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>mice, despite similar colonization levels of WT<jats:sub>Hc<\/jats:sub>in the cecum and colon of both B6 and IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>mice. WT<jats:sub>Hc<\/jats:sub>and<jats:italic>cdtB<\/jats:italic>mutants also colonized IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>mice to a similar extent, but infection with either<jats:italic>cdtB<\/jats:italic>mutant resulted in attenuated typhlocolitis and hyperplasia compared to infection with WT<jats:sub>Hc<\/jats:sub>(<jats:italic>P<\/jats:italic>&lt; 0.03), and only WT<jats:sub>Hc<\/jats:sub>infection caused dysplasia and intramucosal carcinoma. WT<jats:sub>Hc<\/jats:sub>and<jats:italic>cdtB<\/jats:italic><jats:sub>Hc<\/jats:sub>mutant infection of IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>mice elevated mRNA expression of tumor necrosis factor alpha, inducible nitric oxide synthase, and gamma interferon in the cecum, as well as elevated Th1-associated serum immunoglobulin G2a<jats:sup>b<\/jats:sup>compared to infection of B6 mice (<jats:italic>P<\/jats:italic>&lt; 0.05). Although no hepatitis was noted, liver samples were PCR positive at various time points for WT<jats:sub>Hc<\/jats:sub>or the<jats:italic>cdtB<\/jats:italic><jats:sub>Hc<\/jats:sub>mutant in approximately 33% of IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>mice and in 10 to 20% of WT<jats:sub>Hc<\/jats:sub>-infected B6 mice. These results indicate that WT<jats:sub>Hc<\/jats:sub>can be used to model inflammatory bowel disease in IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>mice and that CDT contributes to the virulence of<jats:italic>H. cinaedi<\/jats:italic>.<\/jats:p>","DOI":"10.1128\/iai.00166-09","type":"journal-article","created":{"date-parts":[[2009,3,24]],"date-time":"2009-03-24T00:55:34Z","timestamp":1237856134000},"page":"2508-2516","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":60,"title":["Cytolethal Distending Toxin Promotes<i>Helicobacter cinaedi<\/i>-Associated Typhlocolitis in Interleukin-10-Deficient Mice"],"prefix":"10.1128","volume":"77","author":[{"given":"Z.","family":"Shen","sequence":"first","affiliation":[{"name":"Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.","family":"Feng","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. 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