Zinc deficiency suppresses alveolar macrophage function in in vivo models of both chronic alcohol ingestion and HIV‐1 transgenic expression

Abstract

Alcohol abuse and HIV‐1 infection independently affect many individuals and render them susceptible to severe pulmonary infections. Alcoholics and HIV‐1 infected individuals are known to be deficient in immunostimulatory micronutrient zinc. Although zinc deficiency is known to have adverse effects on the ciliated epithelium within the upper airway, there is very little known about zinc homeostasis within the alveolar space. In this study, we separately examined alveolar zinc levels and the effect of inadequate zinc microenvironment on alveolar macrophage immune function in chronic alcohol‐fed and hemizygous NL4‐3Δgag/pol transgenic rats. Alveolar epithelial lining fluid from each rat model was significantly zinc deficient. Alveolar macrophages from these rats had significantly fewer granulocyte‐macrophage colony stimulating factor (GM‐CSF) receptors, and significantly reduced capacity to phagocytose bacteria. Zinc supplementation increased pulmonary zinc levels, GM‐CSF receptor expression, and significantly improved phagocytic function of alveolar macrophages in both the models. These data suggest an important role for pulmonary zinc in these two clinical settings that are associated with pneumonia.