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Role of interleukin-10 in a murine model of dextran sulfate sodium-induced colitis.

AbstractBACKGROUND:
Increased production of proinflammatory cytokines is characteristic of both animal models of experimental colitis and human inflammatory bowel disease. This study was designed to characterize the functional role of interleukin (IL)-10 in a murine model of experimental colitis.
METHODS:
Cytokine profiles were analyzed in animals with dextran sulfate sodium-induced colitis. The effect of treatment with IL-10 or anti-IL-10 antibodies on colonic cytokine production in vitro and tissue damage in vivo were evaluated.
RESULTS:
After the induction of colitis, there was a time-dependent increase in tissue tumor necrosis factor-alpha and IL-1beta levels, followed by a peak of the IL-10 level. The production of tumor necrosis factor-alpha and IL-1beta by cultured colonic tissues was inhibited by addition of IL-10, and conversely, it was enhanced by anti-IL-10. Treatment with IL-10 resulted in a marked improvement in intestinal inflammation. Blocking endogenous IL-10 was found to cause a modest exacerbation of inflammation.
CONCLUSIONS:
These results show that IL-10 has a functional role in regulating colonic inflammation during experimental colitis.
AuthorsM Tomoyose, K Mitsuyama, H Ishida, A Toyonaga, K Tanikawa
JournalScandinavian journal of gastroenterology (Scand J Gastroenterol) Vol. 33 Issue 4 Pg. 435-40 (Apr 1998) ISSN: 0036-5521 [Print] England
PMID9605267 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Interleukin-1
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Dextran Sulfate
Topics
  • Animals
  • Colitis (chemically induced, metabolism)
  • Colon (drug effects, metabolism)
  • Dextran Sulfate
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Interleukin-1 (metabolism)
  • Interleukin-10 (metabolism, pharmacology, physiology)
  • Mice
  • Mice, Inbred BALB C
  • Tumor Necrosis Factor-alpha (metabolism)

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