Cigarette smoking increases bronchial mucosal IL‐17A expression in asthmatics, which acts in concert with environmental aeroallergens to engender neutrophilic inflammation

Abstract

The data support the hypothesis that asthmatic smokers develop neutrophilic inflammation of the airways propagated at least partly by smoke-induced production of IL-17A which together with smoke and other environmental stimuli acts on airways epithelial cells to induce neutrophil chemotaxins.