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

作者：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^*

来源：Communications Biology, 2019, 2(1): 33.

DOI：10.1038/s42003-018-0270-9

• NF-KAPPA-B
• DELTA-T-CELLS
• CIGARETTE-SMOKE
• OCULAR SURFACE
• OXIDATIVE STRESS
• IL-6
• ACTIVATION
• MECHANISMS
• EXPRESSION
• NOREPINEPHRINE

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-kappa B (NF-kappa B) and inflammatory molecules such as interleukin-6 (IL-6) and IL-17. We find that chemical SNS sympathectomy, local adrenergic receptor antagonism, NF-kappa B1 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.

• 出版日期2019-1-24
• 单位暨南大学; 河南省眼科研究所; 河南大学; 河南省人民医院