Alcohol, the Upper Airway, and Mucociliary Dysfunction in the Conducting Airways

Abstract

Innate mucosal defense in the airways of the lung involves mucociliary clearance of inhaled particles, microbes, and toxins. Alcohol consumption results in both rapid and transient stimulation of the frequency of cilia beat as well as a prolonged exposure-mediated desensitization of cilia stimulation leading to diminished clearance. This alcohol-induced ciliary dysfunction (AICD) is the result of the direct exposure of the airways to condensed alcohol from the bronchial circulation during exhalation. In addition, alcohol can alter mucus production, pro-inflammatory cytokine release, barrier function, cell migration during wound repair, and smooth muscle airway hyperresponsiveness in exposed airways. Such alterations impact normative airway functions in response to other inhaled injurious agents such as viruses, cigarette smoke, and organic dusts.