Triggering of TLR3 by polyI:C in human corneal epithelial cells to induce inflammatory cytokines

被引:122
|
作者
Ueta, M [1 ]
Hamuro, J
Kiyono, H
Kinoshita, S
机构
[1] Kyoto Prefectural Univ Med, Dept Ophthalmol, Kyoto, Japan
[2] Univ Tokyo, Inst Med Sci, Div Mucosal Immunol, Minato Ku, Tokyo, Japan
基金
日本科学技术振兴机构;
关键词
human corneal epithelial cells; Polyl : C; TLRs; inflammation; LPS;
D O I
10.1016/j.bbrc.2005.02.196
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Epithelial cells of the ocular surface are key in the first-line defense as a part of the mucosal immune system against pathogens. We investigated whether polyI:C induces the production by human corneal epithelial cells (HCEC) of pro-inflammatory cytokines and IFN-beta, and whether Toll-like receptor (TLR)-3 expression is amplified by polyI:C. TLR3 was expressed on the surface of HCEC. Stimulation with polyI:C elicited the elevated production and mRNA expression of IL-6 and IL-8 in HCEC. While polyI:C induced IFN-beta, far stronger than human fibroblasts, and TLR3 gene expression in HCEC, LPS stimulation did not. Similarly, polyI:C, but not LPS, induced the gene expression of I kappa B alpha and MAIL, members of the I kappa B family, in HCEC. The innate immune response of HCEC is distinct from that of immune-competent cells, and we suggest that this is indicative of the symbiotic relationship between corneal epithelium and microbes inhabiting the ocular surface. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:285 / 294
页数:10
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