期刊
JOURNAL OF BIOMEDICAL SCIENCE
卷 26, 期 -, 页码 -出版社
BMC
DOI: 10.1186/s12929-019-0539-4
关键词
Triggering expressed on myeloid cells-1; Inflammatory macrophages; IL-22; Group 3 innate lymphoid cells; Colitis
资金
- MOST in Taiwan [MOST 103-2320-B-010-021-MY3, MOST 106-2320-B-010 -016 -MY3]
- Far Eastern Memorial Hospital National Yang-Ming University Joint Research Program [NYMU-FEMH 105DN16, 106DN16]
- Cancer Progression Research Center, National Yang-Ming University from The Featured Areas Research Center Program within the Ministry of Education (MOE) in Taiwan
BackgroundTriggering receptor expressed on myeloid cells-1 (TREM-1) is highly expressed on macrophages in inflamed intestines and reportedly promotes inflammatory bowel disease (IBD) by augmenting pro-inflammatory responses. To study the mechanism mediated by TREM-1 on macrophages, we generated an independent TREM-1 deficient mouse.MethodsAcute colitis was induced in C57BL/6 and TREM-1-deficient mice by the administration of dextran sodium sulfate (DSS). Colonic lamina propria immune cell composition and cytokines were analyzed. An innate lymphoid cell (ILC) co-culture experiment with macrophages was used to analyze IL-22 levels. Exogenous IL-22 and TREM-1-expressing macrophages were supplied to TREM-1-deficient mice for examining their effects on intestinal barrier integrity.ResultsIn inflamed colons, TREM-1 loss compromised the activation of ILC3 and their production of IL-22, which is required for intestinal barrier integrity. ILC3-mediated IL-22 production depends on IL-1 secreted by M1-polarized macrophages, and we found that TREM-1 deficiency results in a decreased number of IL-1 producing-M1 macrophages in colons exposed to DSS. Accordingly, DSS-mediated damage was ameliorated by supplying exogenous IL-22 and TREM-1-expressing macrophages to TREM-1-deficient mice.ConclusionsTREM-1 plays a crucial role in regulating IL-22 production by ILC3 through modulating M1-macrophage polarization during DSS-induced acute colitis.
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