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Novel urease-negative Helicobacter species associated with colitis and typhlitis in IL-10-deficient mice

  1. Author:
    Fox, J. G.
    Gorelick, P. L.
    Kullberg, M. C.
    Ge, Z. M.
    Dewhirst, F. E.
    Ward, J. M.

  2. Author Address

    Fox JG MIT, Div Comparat Med Cambridge, MA 02139 USA MIT, Div Comparat Med Cambridge, MA 02139 USA NCI, Anim Hlth Diagnost Lab, Lab Anim Sci Program, FCRDC,Sci Applicat Int Corp Frederick, MD 21702 USA NCI, Vet & Tumor Pathol Sect, Anim Sci Branch, Off Lab Anim Resources,Div Basic Sci Frederick, MD 21702 USA NIAID, Immunobiol Sect, Parasit Dis Lab, NIH Bethesda, MD 20892 USA Forsyth Dent Ctr Boston, MA 02115 USA
    1. Year: 1999
  2. Journal: Infection and Immunity
    1. 67
    2. 4
    3. Pages: 1757-1762
  4. Type of Article: Article
  1. Abstract:

    A spiral-shaped bacterium with bipolar, single-sheathed flagella was isolated from the intestines of IL-10 (interleukin-10) deficient (IL-10(-/-)) mice with inflammatory bowel disease. The organism aas microaerobic, grew at 37 and 42 degrees C, and was oxidase and catalase positive but urease negative. On the basis of 16S rRNA gene sequence analysis and biochemical and phenotypic criteria, the organism is classified as a novel helicobacter. Cesarean section-rederived IL-10(-/-) mice without helicobacter infection did not have histological evidence of intestinal inflammation. However, helicobacter-free IL-10(-/-), SCID/NCr, and A/JNCr mice experimentally inoculated with the novel urease-negative Helicobacter sp. developed variable degrees of inflammation in the lower intestine, and in immunocompetent mice, the experimental infection was accompanied by a corresponding elevated immunoglobulin G antibody response to the novel Helicobacter sp. antigen. These data support other recent studies which demonstrate that multiple Helicobacter spp. in both naturally and experimentally infected mice can induce inflammatory bowel disease. The mouse model of helicobacter-associated intestinal inflammation should prove valuable in understanding how specific microbial antigens influence a complex disease process. [References: 29]

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