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Lessons from genetically engineered animal models. XII. IL-10-deficient (IL-10(-/-) mice and intestinal inflammation.

D M Rennick1, M M Fort

  • 1DNAX Research Institute of Cellular and Molecular Biology, Palo Alto, California 94304, USA.

American Journal of Physiology. Gastrointestinal and Liver Physiology
|June 22, 2000
PubMed
Summary

Interleukin-10 deficient mice develop intestinal inflammation due to uncontrolled Th1 cells. Studies explore triggers, mediators, regulatory cells, and Interleukin-10 therapy for inflammatory bowel disease (IBD).

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Area of Science:

  • Immunology
  • Gastroenterology
  • Inflammatory Bowel Disease Research

Background:

  • Interleukin-10 knockout (IL-10(-/-)) mice exhibit spontaneous intestinal inflammation.
  • This inflammation involves transmural lesions and dysregulated cytokine production.
  • Uncontrolled IFN-gamma-producing CD4+ T cells (Th1 type) are implicated in enterocolitis development.

Purpose of the Study:

  • To investigate the role of enteric organisms in triggering intestinal disease in IL-10(-/-) mice.
  • To identify mediators responsible for initiating and maintaining intestinal disease.
  • To examine the function of Interleukin-10 in regulatory cell generation and the efficacy of IL-10 therapy in inflammatory bowel disease (IBD) models.

Main Methods:

  • Studies utilizing IL-10(-/-) mouse models.

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  • Analysis of enteric organisms and inflammatory mediators.
  • Assessment of regulatory cell function.
  • Evaluation of IL-10 therapy in experimental IBD and human patients.

    • Main Results:

    • IL-10(-/-) mice spontaneously develop severe intestinal inflammation.
    • Enteric organisms and specific mediators are identified as key triggers and sustainers of the disease.
    • IL-10 plays a crucial role in regulating immune responses and maintaining gut homeostasis.
    • IL-10 therapy shows potential in managing experimental and human IBD.

    Conclusions:

    • Dysregulated immune responses, particularly Th1-driven inflammation, are central to spontaneous enterocolitis in IL-10(-/-) mice.
    • Understanding the interplay between gut microbiota, immune mediators, and regulatory cells is vital for IBD pathogenesis.
    • IL-10 therapy represents a promising therapeutic strategy for inflammatory bowel disease.