Alcohol Impairment of Granulocyte Function During Lung Infection

Abstract

Heavy alcohol consumption increases the incidence and severity of bacterial pneumonia and other infections. Neutrophil recruitment into the lung is a critical early host response to infection. This chapter focuses on the defects in neutrophil function and production in the alcohol-abusing host. Most of the preclinical literature on this subject has been produced using acute, intoxicating doses of alcohol. These models identify that alcohol-induced suppression of neutrophil recruitment and production are strongly associated with an increased severity of lung infection. Mechanisms responsible for this alcohol-induced granulocyte suppression include decreasing pro-inflammatory cytokine, CXC chemokine, and granulopoietic growth factor production. Neutrophil and/or granulocyte progenitor cell responsiveness to these mediators is also suppressed by alcohol. Additionally, studies indicate that neutrophil functions such as phagocytosis and pathogen killing may also be impaired by severe alcohol intoxication or chronic consumption. Human studies, though fewer in number, identify similar defects imparted by intoxicating concentrations of alcohol. Taken together, present knowledge supports the conclusion that defects in neutrophil recruitment, function and production are pivotal consequences of alcohol abuse and render the host susceptible to a multitude of respiratory infections.