Increased expression of Lysosomal-associated membrane protein 1 (LAMP-1) found in small airway epithelium of COPD may have functional consequence and role in autophagy

Abstract

Aim: Cigarette smoke causes oxidative stress to the lung tissues inducing cellular proteome changes. Cells recycle damaged material using autophagy pathways through the fusion of autophagosomes and lysosomes. However, dysregulation of lysosomes leads to disrupted autophagy and a stressed endoplasmic reticulum (ER). The current study evaluates LAMP-1+ lysosomes in the small airway (SA) epithelium of COPD patients and assess their physiological outcomes. Methods: Tissue SA lung resections from non-smokers (NC), smokers with normal lung function (NLFS), mild-moderate COPD current smokers (CS) and ex-smokers (ES). Staining intensity of LAMP-1+ cells was measured as objects per area of epithelium using an imaging software Image ProPlus and further represented as percent LAMP-1+ expression in SA epithelium. Results: The NC epithelium was devoid of detectable LAMP-1 expression. COPD-CS and NLFS groups showed increase in percent LAMP-1+ lysosomes in the SA epithelium compared to NC (p Conclusions: Our data suggests that smoking stimulates lysosomal accumulation in the SA epithelium and is associated with decrease in lung function in COPD. The consequence of dysregulated lysosomes in COPD warrants further investigations.