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http://dx.doi.org/10.14348/molcells.2018.2123

Cigarette Smoke Extract Enhances IL-17A-Induced IL-8 Production via Up-Regulation of IL-17R in Human Bronchial Epithelial Cells  

Lee, Kyoung-Hee (Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Hospital)
Lee, Chang-Hoon (Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Hospital)
Woo, Jisu (Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Hospital)
Jeong, Jiyeong (Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Hospital)
Jang, An-Hee (Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Hospital)
Yoo, Chul-Gyu (Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Hospital)
Publication Information
Molecules and Cells / v.41, no.4, 2018 , pp. 282-289 More about this Journal
Abstract
Interleukin-17A (IL-17A) is a pro-inflammatory cytokine mainly derived from T helper 17 cells and is known to be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) has been considered as a primary risk factor of COPD. However, the interaction between CS and IL-17A and the underlying molecular mechanisms have not been clarified. In the current study, we investigated the effects of cigarette smoke extract (CSE) on IL-17A-induced IL-8 production in human bronchial epithelial cells, and sought to identify the underlying molecular mechanisms. IL-8 production was significantly enhanced following treatment with both IL-17A and CSE, while treatment with either IL-17A or CSE alone caused only a slight increase in IL-8 production. CSE increased the transcription of IL-17RA/RC and surface membrane expression of IL-17R, which was suppressed by an inhibitor of the phosphoinositide 3-kinase (PI3K)/Akt pathway (LY294002). CSE caused inactivation of glycogen synthase $kinase-3{\beta}$ ($GSK-3{\beta}$) via the PI3K/Akt pathway. Blockade of $GSK-3{\beta}$ inactivation by overexpression of constitutively active $GSK-3{\beta}$ (S9A) completely suppressed the CSE-induced up-regulation of IL-17R expression and the CSE-induced enhancement of IL-8 secretion. In conclusion, inactivation of $GSK-3{\beta}$ via the PI3K/Akt pathway mediates CSE-induced up-regulation of IL-17R, which contributes to the enhancement of IL-17A-induced IL-8 production.
Keywords
Akt; cigarette smoke extract; $GSK-3{\beta}$; IL-17A; IL-17R; IL-8;
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