Resolvin-D1 inhibits interleukin-8 and hydrogen peroxide production induced by cigarette smoke extract in 16HBE cells via attenuating NF-κB activation.

Jiajia Dong; Mingke Zhang; Zenglin Liao; Wei WU; Tao Wang; Lei Chen; Ting Yang; Lingli Guo; Dan XU; Fuqiang Wen

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Resolvin-D1 inhibits interleukin-8 and hydrogen peroxide production induced by cigarette smoke extract in 16HBE cells via attenuating NF-κB activation.

Author: Jiajia DONG ¹ ; Mingke ZHANG ² ; Zenglin LIAO ¹ ; Wei WU ¹ ; Tao WANG ¹ ; Lei CHEN ¹ ; Ting YANG ¹ ; Lingli GUO ¹ ; Dan XU ¹ ; Fuqiang WEN ^{3
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Author Information

1. Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China and Department of Respiratory Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China.
2. Department of Hospital Internal Medicine, Northwest A&F University, Yangling, Shaanxi 712100, China.
3. Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China and Department of Respiratory Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China. Email: wenfuqiang.scu@gmail.com
4. wenfuqiang@126.com.
Publication Type:Journal Article
MeSH: Blotting, Western; Cell Line; Cell Survival; drug effects; Docosahexaenoic Acids; pharmacology; Electrophoretic Mobility Shift Assay; Enzyme-Linked Immunosorbent Assay; Humans; Hydrogen Peroxide; metabolism; Interleukin-8; metabolism; NF-kappa B; metabolism; Reverse Transcriptase Polymerase Chain Reaction; Smoking; adverse effects
From: Chinese Medical Journal 2014;127(3):511-517
CountryChina
Language:English
Abstract:
BACKGROUNDCigarette smoke induced airway inflammation plays a role in pathogenesis of airway inflammation. Resolvin-D1 derived from omega-3 polyunsaturated fatty acids is an endogenous anti-inflammatory and proresolving lipid mediator. Resolvin-D1 ameliorated inflammatory responses in lung injury, asthma, peritonitis and atherosclerosis. We investigated whether resolvin-D1 suppressed the productions of chemokines and oxidative stress induced by cigarette smoke extract (CSE) in vitro and its possible mechanism.
METHODSWe examined the proinflammatory chemokine interleukin-8 and hydrogen peroxide (H2O2) productions induced by CSE in 16 human bronchial epithelial (16HBE) cells after resolvin-D1 treatment and their mechanisms. 16HBE cells were treated with resolvin-D1 at up to 10 nmol/L, for 30 minutes before CSE up to 16% (v/v) exposure. Release of interlukin-8 proteins was assessed by enzyme linked immunosort assay (ELISA) and its mRNA level by RT-PCR. We evaluated extracellular H2O2 expression in the supernatant. Phosphorylation of NF-κB/p65 and degradation of I-κB in 16HBE cells were determined by Western blotting analysis and NF-κB DNA binding activity by electrophoretic mobility shift assay (EMSA).
RESULTS16HBE cells treated with 8% CSE showed significantly higher interlukin-8 production. Resolvin-D1 pretreatment inhibited CSE induced interlukin-8 production (mRNA and protein) in a dose and time dependent manner. Extracellular H2O2 level decreased after resolvin-D1 treatment. Resolvin-D1 attenuated CSE triggered I-κB degradation and NF-κB/p65 activation dose dependently and inhibited NF-κB DNA binding activity.
CONCLUSIONResolvin-D1 inhibits CSE induced interlukin-8 and H2O2 production in 16HBE cells by modulating NF-κB activation and has therapeutic potential for pulmonary inflammation.