Nicotinic α7 acetylcholine receptor (α7nAChR) in human airway smooth muscle

Diseases such as asthma are exacerbated by inflammation, cigarette smoke and even nicotine delivery devices such as e-cigarettes. However, there is currently little information on how nicotine affects airways, particularly in humans, and changes in the context of inflammation or asthma. Here, a longstanding assumption is that airway smooth muscle (ASM) that is key to bronchoconstriction has muscarinic receptors while nicotinic receptors (nAChRs) are only on airway neurons. In this study, we tested the hypothesis that human ASM expresses alpha 7nAChR and explored its profile in inflammation and asthma using ASM of non-asthmatics vs. mild-moderate asthmatics. mRNA and western analysis showed the alpha 7 subunit is most expressed in ASM cells and further increased in asthmatics and smokers, or by exposure to nicotine, cigarette smoke or pro-inflammatory cytokines TNF alpha and IL-13. In these effects, signaling pathways relevant to asthma such as NF kappa B, AP-1 and CREB are involved. These novel data demonstrate the expression of alpha 7nAChR in human ASM and suggest their potential role in asthma pathophysiology in the context of nicotine exposure.

Automated summary

This study found that human ASM cells express alpha 7nAChR receptors, with higher levels in asthmatics and smokers, and further increased by exposure to nicotine, cigarette smoke, or pro-inflammatory cytokines TNF alpha and IL-13. These receptors may play a potential role in asthma pathophysiology through signaling pathways such as NF kappa B, AP-1, and CREB.