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Infection and Immunity, April 1999, p. 1757-1762, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

A Novel Urease-Negative Helicobacter Species Associated with Colitis and Typhlitis in IL-10-Deficient Mice

James G. Fox,1,* Peter L. Gorelick,2 Marika C. Kullberg,3 Zhongming Ge,1 Floyd E. Dewhirst,4 and Jerrold M. Ward5

Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts 021391; Animal Health Diagnostic Laboratory, Laboratory Animal Sciences Program, NCI-FCRDC, Science Applications International Corporation,2 and Veterinary and Tumor Pathology Section, Animal Sciences Branch, Office of Laboratory Animal Resources, Division of Basic Sciences, National Cancer Institute,5 Frederick, Maryland 21702; Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-042513; and Forsyth Dental Center, Boston, Massachusetts 021154

Received 8 October 1998/Returned for modification 11 December 1998/Accepted 23 December 1998

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 was microaerobic, grew at 37 and 42°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.

* Corresponding author. Mailing address: Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA 02139. Phone: (617) 253-1757. Fax: (617) 258-5708. E-mail: jgfox{at}mit.edu.

Infection and Immunity, April 1999, p. 1757-1762, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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