alcohol ingestion causes zinc deficiency within the alveolar space (Joshi et al., 2008). In this study we extended those findings to an experimental model of bacterial pneumonia in vivo and, as expected, alcohol-fed rats showed an increased lung bacterial burden at 24 hours when inoculated with Klebsiella pneumoniae, a common pulmonary pathogen in alcoholics. More importantly, dietary zinc supplementation restored bacterial clearance to levels seen in control-fed rats. The mechanisms for these protective effects are still speculative as we did not directly measure alveolar macrophage host defense in this in vivo pneumonia model. Extrapolating from our in vitro model (Joshi et al., 2008), however, it seems plausible that dietary zinc is augmenting alveolar macrophage immune function. Normal host defenses against lung bacterial infection include both innate and acquired immune responses. The innate response depends on processes such as mucociliary clearance as well as alveolar macrophage recognition and removal of foreign particles and organisms that reach the distal airways and alveolar 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
