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Updated: Feb 5, 2026

Primary Human Bronchial Epithelial Cells Grown from Explants
Published on: March 26, 2010
Carbon Monoxide Inhibits Cytokine and Chloride Secretion in Human Bronchial Epithelia
Rui-Gang Zhang1,2, Chung-Yin Yip2, Wing-Hung Ko2
1Department of Physiology, Basic Medical School, Guangdong Medical University, Guangdong, China.
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-.
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