Bacterial pneumonia is the most common cause of lower respiratory tract infection in immunocompromised populations, including the alcohol-abusing patient. Furthermore, alcoholics are frequently infected with highly virulent respiratory pathogens and consequently experience increased morbidity and mortality from bacterial pneumonia. The resulting increase in health care resource use in these patients represents a significant public health concern. Host defense mechanisms are operant from the nasopharynx to the alveolus, many of which are adversely affected by excessive alcohol intake. Although the increased risk of oropharyngeal aspiration has been recognized for centuries, only recently have detailed studies of the mechanical, innate, and adaptive immune systems identified specific mechanisms throughout the aerodigestive tract whereby ethanol exposure renders the individual more susceptible to infection. In addition to directly inhibiting the ability of resident lung immune cells to kill bacteria, excessive ethanol use suppresses the normally protective acute inflammatory response to infection, resulting in the defective recruitment of additional innate immune cells. Additionally, ethanol disrupts the intricate interface that exists between innate and adaptive pulmonary immunity, further hindering the alcoholic host's ability efficiently to eliminate invading pathogens. Whether immunomodulatory therapies, designed to augment the immune response in such patients, will be effective adjunct therapy in such patients remains to be determined. This article reviews some of the key mechanisms of pulmonary host defense that are negatively impacted in the setting of alcohol abuse.