Acute tobacco smoke exposure exacerbates the inflammatory response to corneal wounds in mice via the sympathetic nervous system

• Published in: Communications biology 2019-01, Vol.2 (1), p.33, Article 33
• Main Authors: Xiao, Chengju, Wu, Mingjuan, Liu, Jun, Gu, Jianqin, Jiao, Xinwei, Lu, Dingli, He, Jingxin, Lin, Cuipei, Xue, Yunxia, Fu, Ting, Wang, Hanqing, Wang, Guang, Yang, Xuesong, Li, Zhijie
• Format: Article
• Language: English
• Subjects: 13/21; 13/31; 13/51; 14/1; 14/63; 38/77; 38/90; 631/250/256; 64/60; 692/308/1426; 692/699/578; Abrasion; Adrenergic receptors; Analysis of Variance; Animals; Biology; Biomarkers; Biomedical and Life Sciences; Cornea; Corneal Injuries - complications; Corneal Injuries - etiology; Cytokines - metabolism; Disease Progression; Disease Susceptibility; Environmental Exposure - adverse effects; Epinephrine - pharmacology; Inflammation; Interleukin 17; Interleukin 6; Keratitis - etiology; Keratitis - metabolism; Keratitis - pathology; Life Sciences; Mice; Nervous system; NF-kappa B - metabolism; NF-κB protein; Public health; Receptors, Antigen, T-Cell, gamma-delta - metabolism; Signal Transduction; Smoke; Sympathetic nervous system; Sympathetic Nervous System - metabolism; T-Lymphocyte Subsets - immunology; T-Lymphocyte Subsets - metabolism; Tobacco; Tobacco smoke; Tobacco Smoke Pollution - adverse effects; Wound healing
• ISSN: 2399-3642; 2399-3642
• DOI: 10.1038/s42003-018-0270-9

Exposure to tobacco smoke is a major public health concern that can also affect ophthalmic health. Based on previous work demonstrating the important role of the sympathetic nervous system (SNS) in corneal wound repair, we postulated that acute tobacco smoke exposure (ATSE) may act through the SNS in the impairment of corneal wound repair. Here we find that ATSE rapidly increases the markers of inflammatory response in normal corneal limbi. After an abrasion injury, ATSE exaggerates inflammation, impairs wound repair, and enhances the expression of nuclear factor-κB (NF-κB) and inflammatory molecules such as interleukin-6 (IL-6) and IL-17. We find that chemical SNS sympathectomy, local adrenergic receptor antagonism, NF-κB1 inactivation, and IL-6/IL-17A neutralization can all independently attenuate ATSE-induced excessive inflammatory responses and alleviate their impairment of the healing process. These findings highlight that the SNS may represent a major molecular sensor and mediator of ATSE-induced inflammation. Chengju Xiao et al. find that acute tobacco smoke exaggerates inflammation in recently wounded mouse corneas, thereby impairing wound repair. They show that the effect of tobacco smoke is mediated by activation of the sympathetic nervous system.