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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. We demonstrated that exposure of J774.16 macrophage-like cells to physiological alcohol (EtOH) concentrations decreased phagocytosis and killing of Ab. EtOH-mediated macrophage phagocytosis dysfunction may be associated with reduced expression of GTPase-RhoA, a key regulator of the actin polymerization signaling cascade. EtOH inhibited nitric oxide (NO) generation via inducible NO-synthase inactivation, which enhanced Ab survival within macrophages. Additionally, EtOH alters cytokine production resulting in a dysregulated immune response. This study is a proof of principle which establishes that EtOH might exacerbate Ab infection and be an important factor enhancing CAP in individuals at risk.
Submitted
05/23/13
Revised
06/26/13
Accepted
07/05/13
Disclosure of Potential Conflicts of Interest
No potential conflicts of interest were disclosed.
Authorship
All authors contributed to the design of the experiments, analysis of the data, and writing of the manuscript. MBA performed the phagocytosis and killing assays, western blot, and cytokine analyses. CC and RJC performed the FACS and microscopy, respectively.
Acknowledgments
LRM is supported by the NIH-NIAID 5K22A108781702 and Long Island University-Post Faculty Research Committee Awards. We thank Dr Joshua D Nosanchuk for his constructive suggestions.