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Am J Physiol Gastrointest Liver Physiol 279: G90-G99, 2000;
0193-1857/00 $5.00
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Vol. 279, Issue 1, G90-G99, July 2000

Spontaneously developing chronic colitis in IL-10/iNOS double-deficient mice

Donna-Marie McCafferty1, Elaine Sihota1, Marcelo Muscara2, John L. Wallace2, Keith A. Sharkey3, and Paul Kubes1

1 Immunology and 3 Neuroscience Research Groups, Department of Physiology and Biophysics, and 2 Gastrointestinal Research Group, Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1

Mice deficient in both inducible nitric oxide synthase (iNOS) and interleukin (IL)-10 (iNOS-/-/IL-10-/-) were created to examine the role of iNOS in spontaneously developing intestinal inflammation. IL-10-/-/iNOS-/- mice were compared with IL-10-/- (iNOS+/+) littermates over 6 mo. RT-PCR, Western blot analysis, and immunohistochemistry were performed to measure iNOS message and protein levels. Plasma nitrate/nitrite (NOx) levels were assessed by HPLC. Damage scores (macroscopic and microscopic) and granulocyte infiltration were assessed. At 3-4 wk, IL-10-/- and IL-10-/-/iNOS-/- mice had no signs of colonic inflammation or granulocyte infiltration. Plasma NOx levels were not different from controls. By 3-4 mo, IL-10-/- mice had increased damage scores and granulocyte infiltration concurrent with increased mRNA and protein synthesis (restricted to the epithelium) for iNOS in intestinal tissues but not other tissues. Plasma NOx levels increased fivefold. Interestingly, in the absence of iNOS induction or increased plasma NOx, iNOS-/-/IL-10-/- mice had damage and granulocyte infiltration equivalent to those observed in IL-10-/- littermates. These data suggest that iNOS does not impact on the development or severity of spontaneous chronic inflammation in IL-10-deficient mice.

inflammatory bowel disease; nitric oxide; intestine; inflammation; myeloperoxidase


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