Interleukin-17 regulates chemokine and gelatinase B expression in fibroblasts to recruit both neutrophils and monocytes

被引:36
作者
Qiu, Zheng
Dillen, Chris
Hu, Jialiang
Verbeke, Hannelien
Struyf, Sofie
Van Damme, Jo
Opdenakker, Ghislain [1 ]
机构
[1] Univ Louvain, Rega Inst Med Res, Immunobiol Lab, B-3000 Louvain, Belgium
关键词
Chemokine; Fibroblast; Monocyte chemotactic protein-1; Interleukin-17; Matrix metalloproteinase; Tissue inhibitor of metalloprotease; IFN-GAMMA; RHEUMATOID-ARTHRITIS; MICROARRAY ANALYSIS; T-CELLS; INFLAMMATION; IL-17; MATRIX-METALLOPROTEINASE-9; STIMULATION; DESTRUCTION; RECEPTORS;
D O I
10.1016/j.imbio.2009.06.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Interleukin 17 (IL-17) is a proinflammatory cytokine, produced only by activated lymphocytes, but with a broad cellular host range. The effects of IL-17 on fibroblasts were investigated by analysis of the induction of chemokine and matrix metalloprotease (MMP) mRNA levels by RT-PCR. IL-17 stimulated CC chemokine (monocyte chemotactic protein-1; MCP-1/JE) and CXC (KC, MIP-2) chemokine and TIMP-1 mRNA expression in fibroblastoid L929 cells. In normal mouse embryonic fibroblasts (MEF) this induction profile by IL-17 was extended with the mRNAs encoding the chemokine granulocyte chemotactic protein-2 (GCP-2) and the proteases MMP-3, MMP-9 and MMP-13. The MMP-9 and GCP-2 induction by IL-17 in MEF, and the absence of induction in L929 cells, were corroborated by gelatin zymography and ELISA, respectively. The induction of MCP-1/CCL2 by IL-17 was confirmed in human diploid fibroblasts. We conclude that IL-17 regulates differentially chemokine and MMP expression by normal and transformed fibroblasts and is indirectly capable of attracting both monocytes and neutrophils to the inflammatory focus. (C) 2009 Elsevier GmbH. All rights reserved.
引用
收藏
页码:835 / 842
页数:8
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