Abstract
Acinetobacter baumannii (Ab) is a common cause of community-acquired pneumonia (CAP) in chronic alcoholics in tropical and sub-tropical climates and associated with a >50% mortality rate. Using a murine model of alcohol (EtOH) administration, we demonstrated that EtOH enhances Ab-mediated pneumonia leading to systemic infection. Although EtOH did not affect neutrophil recruitment to the lungs of treated mice, it decreased phagocytosis and killing of bacteria by these leukocytes leading to increased microbial burden and severity of disease. Moreover, we determined that mice that received EtOH prior to Ab infection were immunologically impaired, which was reflected in increased pulmonary inflammation, sequential dissemination to the liver and kidneys, and decreased survival. Furthermore, immunosuppression by EtOH was associated with deregulation of cytokine production in the organs of infected mice. This study establishes that EtOH impairs immunity in vivo exacerbating Ab infection and disease progression. The ability of Ab to cause disease in alcoholics warrants the study of its virulence mechanisms and host interactions.
Highlights
Acinetobacter baumannii (Ab) is a Gram-negative bacterium that has gained particular notoriety as one of the leading causes of nosocomial infections, principally amongst immunocompromised individuals [1]
EtOH abuse has been previously shown to predispose the host to communityacquired pneumonia (CAP), to multi-drug resistant Ab resulting in significant illness and mortality [2]
We demonstrated that EtOH administration had a profound effect on survival in mice i.n. challenged with Ab
Summary
Acinetobacter baumannii (Ab) is a Gram-negative bacterium that has gained particular notoriety as one of the leading causes of nosocomial infections, principally amongst immunocompromised individuals [1]. Ab is a primary agent for communityacquired pneumonia (CAP), in individuals with a history of alcohol (EtOH) abuse who characteristically present a fulminant clinical course with secondary bloodstream infection and a .50% mortality rate in tropical and sub-tropical climates [2]. Excess EtOH consumption may lead to host’s innate and acquired immune deficiency, causing increased susceptibility to infections [7,8]. Acute and chronic EtOH abuse alters the capacity of monocytes to present antigens to T-cells [11] as well as adversely modifying the levels of pro-inflammatory cytokines produced by phagocytes [12]. Inflammatory mediators are negatively regulated by immune cells following EtOH exposure [15]
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