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Chemokine CXCL11 links microbial stimuli to intestinal inflammation
Author(s) -
Liu Z.,
Chen X.,
Wang X.,
Song C.H.,
Du Y.,
Su J.,
Yaseen S. A.,
Yang P.C.
Publication year - 2011
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.2011.04382.x
Subject(s) - chemokine , immunology , inflammation , cxcl11 , biology , medicine , chemokine receptor
Summary Interleukin (IL)‐17 plays an important role in the pathogenesis in a number of immune inflammatory disorders. This study aims to investigate the mechanism by which microbial product flagellin is involved in the development of T helper type (Th)17 cells. Serum levels of IL‐17 and CXCL9‐11 in patients with ulcerative colitis (UC) were evaluated. The source and mechanism of CXC11 release in intestinal mucosa were examined with colonic biopsies from UC patients and a colitis mouse model. The role of flagellin in the development of Th17 cells was studied with a cell co‐culture system. High serum levels of CXCL11 and IL‐17 were observed in UC. Flagellin could induce the production of CXCL11 in CD14 + cells that facilitated the development of Th17 cells. In a skewed Th1 response environment flagellin induces intestinal inflammation, with IL‐17 expression predominant. CXCR3/CXCL11 pathway is involved in microbial product flagellin‐induced intestinal inflammation in which the Th17 response plays an important role.

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