Cigarette smoke decreases the expression of secretory component in human bronchial epithelial cells, in vitro

Epithelial secretory component (SC) is thought to be essential for immunologic protection of the respiratory tract from viral and bacterial infection, since it transports polymeric IgA from the basolateral to the luminal surface of epithelial cells. We have hypothesized that recurrent infection in airways of cigarette smokers is at least partly a consequence of cigarette smoke-induced downregulation of the expression and/or release of SC from airway epithelial cells, subsequently resulting in decreased transcytosis of secretory IgA to the airway lumen. To test this hypothesis, we have cultured human bronchial epithelial cells (HBEC) from surgical tissues and exposed these for 20 minutes to either air or cigarette smoke. Following exposure to cigarette smoke the HBEC cultures were incubated for a further period of up to 24 h, during which time separate cultures were processed by immunocytochemistry for the presence of SC, in a time-dependent manner. The stained HBEC cultures were evaluated by colour image analysis for the percentage of total cells staining for SC. Exposure to cigarette smoke significantly decreased the percentage of total HBEC staining for secretory component from a baseline value (median and interquartile[IQ]1, IQ3) of 35.9% (26.5, 41.6) to 15.7% (8.2, 25.4; p < 0.05) 1 h after exposure, compared with exposure to air. The percentage of cells staining for secretory component were further reduced to 5.3% (3.3, 6.4; p < 0.01), 6 h after exposure, compared to exposure to air. After incubation for 24 h following exposure to cigarette smoke, there was gross cell damage and the cells were not suitable for immunocytochemical analysis. These results suggest that short-term exposure to cigarette smoke may compromise the immune barrier function of the airway mucosa by decreasing the expression and/or release of epithelial SC, thereby decreasing the transcytosis of IgA necessary for inactivating the microbial pathogens in the airway lumen.