Carbon Monoxide Inhibits Cytokine and Chloride Secretion in Human Bronchial Epithelia

Cellular Physiology and Biochemistry

Rui-Gang Zhang¹ 

关键词: Carbon monoxide;    Anti-inflammatory;    Purinergic signalling;    Chloride secretion;    Calcium increase;    Heme oxygenase;   

DOI  :  10.1159/000493026

学科分类：分子生物学，细胞生物学和基因

来源: S Karger AG

【 摘 要 】

Background/Aims Carbon monoxide (CO) is an important gas produced endogenously by heme oxygenase (HO) that functions as an anti-inflammatory and in ion channel modulation, but the effects of CO on airway inflammation and ion transport remains unclear. Methods The effect of CO on cell damage- and nucleotide-induced pro-inflammatory cytokine release in primary human bronchial epithelia cells (HBE) and in the 16HBE14o- human bronchial epithelial cell line were investigated. The effects of CO on calcium- and cAMP-dependent chloride (Cl-) secretion were examined using a technique that allowed the simultaneous measurement and quantification of real-time changes in signalling molecules (cAMP and Ca2+) and ion transport in a polarised epithelium. Results CO suppressed the release of interleukin (IL)-6 and IL-8 and decreased the phosphorylation of ERK1/2 and NF-κB p65. Furthermore, CO inhibited UTP-induced increases in calcium and Cl- secretion, and forskolin-induced increases in cAMP and Cl- secretion. Conclusions These findings suggest a novel anti-inflammatory role of CO in human bronchial epithelia via interactions with purinergic signalling pathways. Further, CO modulated both the Ca2+- and cAMP-dependent secretion of Cl-.

【 授权许可】

CC BY-NC-ND