期刊
INFLAMMATORY BOWEL DISEASES
卷 20, 期 5, 页码 835-846出版社
OXFORD UNIV PRESS INC
DOI: 10.1097/MIB.0000000000000033
关键词
chitinase; STAT3; cytokine; intestinal epithelial cells
资金
- National Institutes of Health [R01-DK80070]
- Broad Medical Foundation
- American Gastroenterological Association Foundation
- A*STAR Graduate Academy (Singapore)
- I-A
- National Research Foundation of Korea
Background: Chitinase 3-like 1 (CHI3L1) is an inducible molecule on intestinal epithelial cells during the development of inflammatory bowel disease. Methods: To investigate the role of CHI3L1 in bacterial infectious colitis, we orally inoculated pathogenic Salmonella typhimurium and potentially pathogenic adherent-invasive Escherichia coli (AIEC) LF82 virulent strain into C57Bl/6 wild-type mice or CHI3L1 knockout (KO) mice. Results: Both S. typhimurium and AIEC LF82 were found to efficiently induce severe intestinal inflammation in wild-type mice but not in CHI3L1 KO mice. These bacteria-infected CHI3L1 KO mice exhibit decreased cellular infiltration, bacterial translocation, and production of interleukin (IL)-6 and IL-22, as compared with those of wild-type mice. More importantly, CHI3L1 KO mice displayed aberrant STAT3 activation after bacterial infections. Co-stimulation of CHI3L1 and IL-6, but not IL-22, synergistically activates STAT3 signaling pathway in intestinal epithelial cells in an NF-kappa B/MAPK-dependent manner. Conclusions: CHI3L1 promotes the onset of selected gram-negative bacterial infectious colitis through IL-6/STAT3 pathway.
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