Synergism Between Interleukin (IL)-17 and Toll-like Receptor 2 and 4 Signals to Induce IL-8 Expression in Cystic Fibrosis Airway Epithelial Cells

被引:27
|
作者
Mizunoe, Shota [1 ,2 ]
Shuto, Tsuyoshi [1 ]
Suzuki, Shingo [1 ]
Matsumoto, Chizuru [1 ]
Watanabe, Kenji [1 ,2 ]
Ueno-Shuto, Keiko [3 ]
Suico, Mary Ann [1 ]
Onuki, Kouhei [1 ,2 ]
Gruenert, Dieter C. [4 ,5 ,6 ,7 ,8 ,9 ,10 ]
Kai, Hirofumi [1 ]
机构
[1] Kumamoto Univ, Dept Mol Med, Grad Sch Pharmaceut Sci, Global COE Cell Fate Regulat Res & Educ Unit, Kumamoto 8620973, Japan
[2] Japan Soc Promot Sci, Tokyo 1028472, Japan
[3] Sojo Univ, Pharmacol Lab, Fac Pharmaceut Sci, Kumamoto 8600082, Japan
[4] Univ Calif San Francisco, Dept Otolaryngol Head & Neck Surg, San Francisco, CA 94115 USA
[5] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94115 USA
[6] Univ Calif San Francisco, Eli & Edythe Broad Ctr Regenerat Med & Stem Cell, San Francisco, CA 94115 USA
[7] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94115 USA
[8] Univ Calif San Francisco, Inst Human Genet, San Francisco, CA 94115 USA
[9] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94115 USA
[10] Univ Vermont, Coll Med, Dept Pediat, Burlington, VT 05405 USA
基金
日本学术振兴会;
关键词
interleukin (1L)-17; toll-like receptor 2 and 4 (TLR2/TLR4); IL-8; cystic fibrosis (CF); p38; HOST-DEFENSE; MESSENGER-RNA; PSEUDOMONAS-AERUGINOSA; P38; IL-17A; INFLAMMATION; ACTIVATION; MECHANISMS; STABILITY; ASTHMA;
D O I
10.1254/jphs.11240FP
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Cystic fibrosis (CF) is the most common lethal inherited disorder and is caused by mutations in the gene encoding the CF transmembrane regulator (CFTR). The CF lung expresses a profound proinflammatory phenotype that appears to be related to a constitutive hypersecretion of interleukin (IL)-8 from airway epithelial cells in response to microbial infection. Since overproduction of IL-8 in CF contributes to massive bronchial infiltrates of neutrophils, identification of the pathways underlying IL-8 induction could provide novel drug targets for treatment of neutrophil-dominated inflammatory diseases such as CF. Here, we show that IL-17A synergistically increases 1L-8 production induced by a toll-like receptor (TLR) 2 agonist, peptidoglycan (PGN), or TLR4 agonist, lipopolysaccharide (LPS), in a human CF bronchial epithelial cell line (CFBE41o-). A strong synergism was also observed in primary human CF bronchial epithelial cells, but not in human non-CF cell lines and primary cells. Notably, despite the induction of nuclear factor-kappa B and MAP kinases during TLR2 or TLR4 activation in CFBE41o-, IL-17A-dependent synergism appears to be the result of enhanced PGN- or LPS-induced phosphorylation of p38. Taken together, these studies provide evidence that IL-17A is a critical factor in increasing IL-8 expression in bacteria-infected CF airways via a pathway that regulates p38 phosphorylation.
引用
收藏
页码:512 / 520
页数:9
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