Ontology type: schema:ScholarlyArticle Open Access: True
2004-09-27
AUTHORSManabu Shiraki, Hiroyuki Aihara, Yoshitaka Kinouchi, Seiichi Takahashi, Motoji Oki, Mitsunori Noguchi, Kazuma Takahashi, Jun-ichi Miyazaki, Tooru Shimosegawa
ABSTRACTT-helper-1 (Th1) cytokines play an important role in Crohn's disease, and interleukin-12 (IL-12), which is composed of two subunits, p40 and p35, drives Th1 differentiation. In previous reports, IL-12 p40 was shown to prevent IL-12 from binding to the receptor. We demonstrate here the effect of IL-12 p40 overexpression in intestinal epithelia on enterocolitis mediated by Th1 cells in IL-10-deficient (IL-10−/−) mice on a C57BL/6J background. IL-10 deficient (IL-10−/−)/T3b-IL-12 p40+ (IL-12 p40+) mice and IL-10−/−/T3b-IL-12 p40− (IL-12 p40−) mice were generated by crossing T3b-IL-12 p40 transgenic mice and IL-10−/− mice. At 8 weeks of age, IL-12 p40+ mice did not show any clinical manifestations of colitis. The colon length of IL-12 p40− mice became shorter than that of IL-12 p40+ mice. The histological score of IL-12 p40+ mice was lower. Interferon-gamma (IFN-γ) production was suppressed in both the mesenteric lymph node cell culture and colon tissue culture of IL-12 p40+ mice. There was no significant difference in IL-4 production and tumor necrosis factor-alpha (TNF-α) production between the two groups. These results show that overexpression of IL-12 p40 in intestinal epithelia prevents enterocolitis in IL-10−/− mice by suppressing IFN-γ production, and suggest a potential clinical application of IL-12 p40 for Crohn's disease. Furthermore, these results also suggest that local gene transduction in the intestinal epithelium may be a potent therapeutic approach for Crohn's disease. More... »
PAGES1491-1500
http://scigraph.springernature.com/pub.10.1038/labinvest.3700175
DOIhttp://dx.doi.org/10.1038/labinvest.3700175
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PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/15448706
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