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题名: Crotonaldehyde-exposed macrophages induce IL-8 release from airway epithelial cells through NF-kappa B and AP-1 pathways
作者: Yang, Bi-cheng1, 2;  Yang, Zhi-hua3;  Pan, Xiu-jie3;  Xiao, Feng-jun3;  Liu, Xing-yu4;  Zhu, Mao-xiang3;  Xie, Jian-ping2
关键词: Crotonaldehyde ;  IL-8 ;  NF-kappa B ;  AP-1 ;  Macrophages ;  Airway epithelial cells
刊名: TOXICOLOGY LETTERS
发表日期: 2013-05-10
DOI: 10.1016/j.toxlet.2013.02.018
卷: 219, 期:1, 页:26-34
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology ;  Life Sciences & Biomedicine
类目[WOS]: Toxicology
研究领域[WOS]: Toxicology
英文摘要: Crotonaldehyde, a highly toxic alpha, beta-unsaturated aldehyde, is a major component of cigarette smoke and a ubiquitous environmental pollutant. Crotonaldehyde exposure is known to have adverse effects on respiratory health, but the underlying mechanisms remain obscure. To examine the interaction between macrophages and airway epithelial cells after exposure to crotonaldehyde, BEAS-2B and A549 cells were treated with conditioned media from a human monocytic leukemia cell line (THP-1) cells stimulated with crotonaldehyde. We demonstrate that conditioned media from THP-1 cells stimulated with crotonaldehyde increased interleukin (IL)-8 production, enhanced nuclear factor (NF)-kappa B and AP-1 DNA-binding activity in BEAS-2B and A549 cells. Analysis of these conditioned media revealed marked increases in tumor necrosis factor (TNF)-alpha, IL-1 beta and IL-8 levels. Preincubation of conditioned media with either TNF-alpha- or IL-1 beta-neutralizing antibodies reduced IL-8 production. Furthermore, BEAS-2B and A549 cells directly treated with crotonaldehyde induced increase in IL-8 production. These data suggest that crotonaldehyde is capable of directly stimulating the production of IL-8 in both macrophages and airway epithelial cells. Crotonaldehyde-stimulated macrophages also amplify the inflammatory response by enhancing IL-8 release from airway epithelial cells mediated by NF-kappa B and AP-1 pathways through a mechanism involving TNF-alpha and IL-1 beta. These findings indicate that crotonaldehyde can cause lung inflammatory response via multiple mechanisms, and may contribute to chronic airway inflammation in smokers. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
关键词[WOS]: TUMOR-NECROSIS-FACTOR ;  OBSTRUCTIVE PULMONARY-DISEASE ;  ACTIVATED PROTEIN-KINASES ;  CIGARETTE-SMOKE EXTRACT ;  GENE-EXPRESSION ;  ALPHA,BETA-UNSATURATED ALDEHYDES ;  PROINFLAMMATORY RESPONSE ;  INFLAMMATORY RESPONSE ;  FACTOR-ALPHA ;  TNF-ALPHA
语种: 英语
WOS记录号: WOS:000317348100004
Citation statistics: 
内容类型: 期刊论文
URI标识: http://cas-ir.dicp.ac.cn/handle/321008/137939
Appears in Collections:中国科学院大连化学物理研究所_期刊论文

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作者单位: 1.Chinese Acad Sci, Dalian Inst Chem Phys, Dalian 116023, Liaoning, Peoples R China
2.CNTC, Zhengzhou Tobacco Res Inst, Zhengzhou 450001, Henan, Peoples R China
3.Beijing Inst Radiat Med, Dept Radiat Toxicol & Oncol, Beijing 100850, Peoples R China
4.Shanghai Tobacco Corp, Ctr Technol, Beijing Work Stn, Beijing 101121, Peoples R China

Recommended Citation:
Yang, Bi-cheng,Yang, Zhi-hua,Pan, Xiu-jie,et al. Crotonaldehyde-exposed macrophages induce IL-8 release from airway epithelial cells through NF-kappa B and AP-1 pathways[J]. TOXICOLOGY LETTERS,2013,219(1):26-34.
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