Alcohol impairs J774.16 macrophagelike cell antimicrobial functions in Acinetobacter baumannii infection

Melissa B. Asplund, Carolina Coelho, Radames J.B. Cordero, Luis R. Martinez

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Acinetobacter baumannii (Ab) is a common cause of community-acquired pneumonia (CA P) 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 CA P in individuals at risk.

Original languageEnglish (US)
Pages (from-to)467-472
Number of pages6
Issue number6
StatePublished - 2013
Externally publishedYes


  • Acinetobacter baumannii
  • Alcohol
  • Cytokines
  • Macrophages
  • Phagocytosis

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Microbiology (medical)
  • Infectious Diseases


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