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Spontaneously developing chronic colitis in IL-10/iNOS double-deficient mice
D M McCafferty1, E Sihota, M Muscara
1Immunology, Department of Physiology and Biophysics, University of Calgary, Alberta, Canada.
Summary
Inducible nitric oxide synthase (iNOS) does not influence the development or severity of chronic intestinal inflammation in interleukin-10 (IL-10)-deficient mice. These findings suggest iNOS plays a limited role in this specific model of inflammatory bowel disease.
Area of Science:
- Gastroenterology
- Immunology
- Molecular Biology
Background:
- Interleukin-10 (IL-10) deficiency is linked to spontaneous intestinal inflammation.
- Inducible nitric oxide synthase (iNOS) is implicated in inflammatory processes.
Purpose of the Study:
- To investigate the role of iNOS in the spontaneous development of intestinal inflammation in IL-10-deficient mice.
Main Methods:
- Generation of IL-10(-/-)/iNOS(-/-) mice and comparison with IL-10(-/-) littermates.
- Assessment of iNOS expression via RT-PCR, Western blot, and immunohistochemistry.
- Measurement of plasma nitrate/nitrite (NO(x)) levels using HPLC and evaluation of intestinal damage and granulocyte infiltration.
Main Results:
- IL-10(-/-)/iNOS(-/-) mice exhibited no significant difference in intestinal inflammation or granulocyte infiltration compared to IL-10(-/-) mice.
- iNOS expression and plasma NO(x) levels increased in IL-10(-/-) mice by 3-4 months but not in the double knockout group.
- Despite the absence of iNOS induction, the iNOS(-/-)/IL-10(-/-) mice showed comparable levels of damage and infiltration.
Conclusions:
- iNOS does not appear to impact the development or severity of spontaneous chronic intestinal inflammation in IL-10-deficient mice.
- The study suggests that other factors may be more critical in driving intestinal inflammation in this model.