Chronic alcohol abuse causes discrete changes in the alveolar macrophages that render
the lung susceptible to serious infections such as tuberculosis. Many studies done in relevant animal
models have identified common mechanisms by which alcohol abuse targets not only the alveolar
macrophage but also the alveolar epithelium, thus resulting in lung injury. One of the mechanisms
by which chronic alcohol ingestion results in oxidative stress is by decreasing the levels of the
antioxidant glutathione within the alveolar space. Other studies have focused on depletion of
essential micronutrients such as zinc that is also linked to oxidative stress mediated cellular
dysfunction. These changes in the pulmonary microenvironment adversely affect granulocyte/
macrophage colony stimulating factor (GM-CSF) signaling in the alveolar macrophage, and
thereby, dampens its function. Although the oxidative stress related changes are often subclinical
and only lead to lung impairment when challenged by an acute insult such as trauma or sepsis,
macrophage dysfunction at the cellular and the molecular levels is often evident in otherwise
healthy alcoholics. In addition, chronic alcohol abuse increases the frequency and severity of
ventilator-associated pneumonia, and increases susceptibility to viral infections such as HIV/AIDS.
Thus, an understanding of the effects of chronic alcohol abuse on the function of alveolar
macrophage has significant potential to identify new innovative treatments that could reduce the
increased morbidity and mortality in this vulnerable population.
Keywords: Macrophages, immune response, pulmonary, infections, oxidative stress.
