Helicobacter hepaticusDoes Not Induce or Potentiate Colitis in Interleukin-10-Deficient Mice

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Abstract
Helicobacter hepaticushas been reported to induce colitis, hepatitis, and hepatocellular carcinoma in several different murine models. The aim of this study was to determine ifH. hepaticuswill cause colitis in monoassociated mice lacking the interleukin-10 gene (IL-10−/−mice) and potentiate colitis in specific-pathogen-free (SPF) IL-10−/−mice. Germfree IL-10−/−mice on either a mixed (C57BL/6 × 129/Ola) or inbred (129/SvEv) genetic background were monoassociated withH. hepaticusATCC 51448 by oral feeding and rectal enemas. In a second experiment, germfree IL-10−/−mice were colonized with stool from SPF mice that harbored or did not harbor endogenousH. hepaticus. After 7 to 9 weeks of colonization, weight loss and mortality were assessed, the colon was isolated for histology and IL-12 secretion, and mesenteric lymph node cells were assessed for T-cell activation markers. It was found that IL-10−/−mice monoassociated withH. hepaticusfor up to 16 weeks showed almost no histologic colitis or increased IL-12 production. SPF IL-10-knockout mice had no significant difference in weight loss, mortality rate, histologic scores, colonic IL-12 secretion, or T-cell activation with or withoutH. hepaticus. We conclude thatH. hepaticusdoes not induce or potentiate disease in our IL-10−/−mice and therefore is not required to induce colitis in genetically susceptible hosts.