Abstract

We previously reported that chronic expression of HIV‐1‐related proteins in an HIV‐1 transgenic rat (HIV‐1 Tg) model altered the expression and membrane localization of the tight junction proteins, occludin and ZO‐1 in the alveolar epithelium, and decreased lung liquid clearance in vivo. Alcohol abuse and HIV‐1 infection frequently co‐exist and these individuals are at high risk for serious lung infections and respiratory failure. Therefore, in this study we evaluated the potential additive effects of alcohol ingestion on alveolar epithelial barrier dysfunction caused by chronic expression of HIV‐1‐related proteins. Chronic alcohol ingestion (6 wks) worsened lung liquid clearance in vivo and exacerbated paracellular permeability in vitro in HIV‐1 Tg rats. Further, immunoblotting and immunocytofluorescence analyses of tight junction protein expression in primary alveolar epithelial cells showed that the decrease in occludin and ZO‐1 expression was more pronounced in alcohol‐fed rats. In addition, by qPCR analysis, alcohol significantly suppressed epithelial sodium channel expression, which would be predicted to impair alveolar epithelial sodium transport. These findings suggest that alcohol ingestion augments HIV‐1‐induced defects in the alveolar epithelial barrier, which could explain the increased risk of respiratory failure in these vulnerable individuals.

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