Autophagy is involved in allergic rhinitis by inducing airway remodeling.

Abstract

Allergic rhinitis (AR) is an allergic disorder affecting 10-40% of the population worldwide. Autophagy has been implicated in numerous biological processes, including aging, immunity, development, and differentiation, and has been shown to affect the pathogenesis of allergic disease and airway remodeling. In this study we attempted to determine the association between autophagy and AR pathogenesis. The severity of nasal and extranasal symptoms was measured with visual analog scale (VAS) scores. Autophagosome formation was detected in the nasal epithelium by transmission electron microscopy (TEM). Western blots and quantitative polymerase chain reaction were used to examine expression levels of autophagic markers. Collagen deposition was detected via Masson trichrome staining and collagen III expression was measured by enzyme-linked immunosorbent assay. Spearman's correlation coefficient was used to assess the relationship between autophagy, AR symptoms, and collagen levels. Patients with AR had more autophagosomes, increased levels of Beclin-1 mRNA, and higher Beclin-1 and LC3-II protein expression. Collagen III protein expression was also higher in patients with AR than in the controls. Higher expression of Beclin-1 was associated with higher VAS scores (Spearman's rho = 0.905, p < 0.01), higher collagen deposition (Spearman's rho = 0.862, p < 0.01), and higher collagen III protein (Spearman's rho = 0.849, p < 0.01). The autophagosome and autophagic markers are highly expressed in the upper airways of patients with AR and are associated with corresponding changes in airway remodeling markers. Our data suggest a link between autophagy and airway remodeling in AR.