space, and bacterial clearance models have long been used as a surrogate measure of host innate immune response (Karaolis et al., 2007;Lehner et al., 2001). Both phagocytosis and intracellular killing of ingested organisms are essential functions of the alveolar macrophage that are impaired by chronic alcohol ingestion. Moreover, experimental models have shown alcohol to impair mucociliary clearance while recent evidence may suggest that zinc may enhance it (Woodworth et al., 2010). Although not tested in our study, this may represent another potential mechanism by which zinc supplementation improves bacterial clearance in alcohol-fed rats. It is reasonable to postulate that zinc deficiency, as a consequence of alcoholism, contributes to innate immune dysfunction, and zinc supplementation could confer protection to this vulnerable population.
