Laryngeal mucus hypersecretion is exacerbated after smoking cessation and ameliorated by glucocorticoid administration

- Cigarette smoke solution (CSS) induces laryngeal mucus hypersecretion.
- Short-term smoking cessation further exacerbates mucus hypersecretion with the upregulation of inflammatory cytokines.
- Long-term smoking cessation is effective to suppress mucus hypersecretion and inflammation.
- Triamcinolone suppresses this inflammation and CSS-induced laryngeal mucus hypersecretion.

IntroductionThe mechanisms underlying the effects of cigarette smoke and smoking cessation on respiratory secretion, especially in the larynx, remain unclear.ObjectivesThe aims of this study were to determine the effects of cigarette smoke and smoking cessation on laryngeal mucus secretion and inflammation, and to investigate the effects of glucocorticoid administration.MethodsWe administered cigarette smoke solution (CSS) to eight-week-old male Sprague Dawley rats for four weeks, then examined laryngeal mucus secretion and inflammatory cytokine expression on days 1, 28 and 90 after smoking cessation. We also investigated the effects of the glucocorticoid triamcinolone acetonide when administered on day 1 after smoking cessation.ResultsExposure to CSS resulted in an increase in laryngeal mucus secretion that was further excacerbated following smoking cessation. This change coincided with an increase in the expression of mRNA for the inflammatory cytokines tumor necrosis factor and interleukin-6, as well as mRNA for MUC5AC, which is involved in mucin production. Triamcinolone suppressed CSS-induced laryngeal mucus hypersecretion and pro-inflammatory cytokine production.ConclusionCigarette smoke-associated inflammation may contribute to the exacerbated laryngeal mucus hypersecretion that occurs following smoking cessation. The inflammatory response represents a promising target for the treatment of cigarette smoke-associated mucus hypersecretion.