There are numerous descriptions of alcohol-induced dysfunction of the immune system (von et al., 2002;Szabo and Mandrekar, 2009;Szabo et al., 2007). Specifically within the respiratory system, individuals with alcohol use disorders are prone to aspiration, have decreased mucociliary clearance, and have impaired host immunity in the airways (Happel and Nelson, 2005;Joshi and Guidot, 2007). We have previously shown that chronic alcohol ingestion has detrimental effects on alveolar macrophage immune function and alveolar epithelial barrier function in experimental animals (Guidot et al., 2000;Joshi et al., 2005) These findings build on prior reports that resident alveolar macrophages in alcoholics are impaired not only in their ability to phagocytose bacteria, but also in their release of cytokines, chemokines, and other factors responsible for microbial killing (D’Souza et al., 1995;D’Souza et al., 1996;Mason et al., 2000;Standiford and Danforth, 1997;Zhang et al., 1999). Recent studies from our alcohol research group implicate a defect in signaling by granulocyte/monocyte colony-stimulating factor (GM-CSF), which is integral to macrophage maturation, differentiation and function. We determined that chronic alcohol ingestion decreases GM-CSF receptor expression and signaling capacity through its master
