期刊
IMMUNOLOGY
卷 151, 期 4, 页码 433-450出版社
WILEY
DOI: 10.1111/imm.12741
关键词
ficolin-2; ficolin-A; inflammatory bowel disease; macrophage; Toll-like receptor 4
类别
资金
- National Natural Science Foundation of China [31221061, 31270176, 31370197]
- National Outstanding Youth Foundation of China [81025008]
- Hubei Province's Outstanding Medical Academic Leader Programme [523-276003]
- Hubei Province Major Knowledge Innovation Project (Natural Science Foundation) [2016CFA062]
- Hubei Province Technological Innovation Special Foundation Major Project [2016ACA150]
- Science and Technology Program of Wuhan [201150530141]
Human ficolin-2 (FCN-2) and mouse ficolin-A (FCN-A, a ficolin-2-like molecule in mouse) are activators of the lectin complement pathway, present in normal plasma and usually associated with infectious diseases, but little is known about the role of FCN-A/2 in inflammatory bowel disease (IBD). In our present study, we found that patients with IBD exhibited much higher serum FCN-2 levels than healthy controls. In the dextran sulphate sodium-induced acute colitis mouse model, FCN-A knockout mice showed much milder disease symptoms with less histological damage, lower expression levels of pro-inflammatory cytokines [interleukin-6 (IL-6), IL-1 and tumour necrosis factor- (TNF-)], chemokines (CXCL1/2/10 and CCL4) and higher levels of the anti-inflammatory cytokine IL-10 compared with wild-type mice. We demonstrated that FCN-A/2 exacerbated the inflammatory pathogenesis of IBD by stimulating M1 polarization through the TLR4/MyD88/MAPK/NF-B signalling pathway in macrophages. Hence, our data suggest that FCN-A/2 may be used as a novel therapeutic target for IBD.
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