title: Alcohol impairs J774.16 macrophage-like cell antimicrobial functions in Acinetobacter baumannii infection.
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.
authors.affiliation: Department of Biomedical Sciences, Long Island University-Post, Brookville, NY, USA.
authors.forename: Melissa B
authors.initials: MB
authors.lastname: Asplund
authors.forename: Carolina
authors.initials: C
authors.lastname: Coelho
authors.forename: Radames J B
authors.initials: RJ
authors.lastname: Cordero
authors.forename: Luis R
authors.initials: LR
authors.lastname: Martinez
mesh_terms: D000151:Acinetobacter Infections / Q000276:immunology* / Q000382:microbiology; D040981:Acinetobacter baumannii / Q000502:physiology*; D000438:Alcohols / Q000494:pharmacology*; D000818:Animals; D002460:Cell Line; D016207:Cytokines / Q000276:immunology; D006801:Humans; D008264:Macrophages / Q000187:drug effects* / Q000276:immunology*; D051379:Mice; D009569:Nitric Oxide / Q000276:immunology; D010587:Phagocytosis / Q000187:drug effects*
chemical_list: D000438:Alcohols; D016207:Cytokines; D009569:Nitric Oxide
keywords: Acinetobacter baumannii; alcohol; cytokines; macrophages; phagocytosis