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Related Experiment Videos

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.

American Journal of Physiology. Gastrointestinal and Liver Physiology
|July 18, 2000
PubMed
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.

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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:

Related Experiment Videos

  • 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.