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Published on: November 15, 2024
Alcohol impairs J774.16 macrophage-like cell antimicrobial functions in Acinetobacter baumannii infection
Melissa B Asplund1, Carolina Coelho, Radames J B Cordero
1Department of Biomedical Sciences, Long Island University-Post, Brookville, NY, USA.
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.
Insights
Chronic alcohol consumption impairs macrophage function, hindering the body's ability to fight Acinetobacter baumannii pneumonia. This alcohol-induced immune dysfunction increases the risk and severity of this dangerous infection.
Area of Science:
- Immunology
- Microbiology
- Toxicology
Background:
- Acinetobacter baumannii (Ab) causes severe community-acquired pneumonia (CAP), especially in chronic alcoholics.
- This infection carries a high mortality rate (>50%) in at-risk populations.
- The impact of alcohol on the immune response to Ab is not fully understood.
Purpose of the Study:
- To investigate the effects of alcohol (ethanol, EtOH) on macrophage function and immune response during Ab infection.
- To elucidate the mechanisms by which EtOH may exacerbate Ab-induced CAP.
Main Methods:
- Exposure of macrophage-like cells (J774.16) to physiological ethanol concentrations.
- Assessment of macrophage phagocytosis and killing of Ab.
- Measurement of GTPase-RhoA expression, nitric oxide (NO) generation, and inducible NO-synthase (iNOS) activity.
- Analysis of cytokine production.
Main Results:
- Ethanol significantly decreased macrophage phagocytosis and killing of Ab.
- EtOH exposure reduced GTPase-RhoA expression, impacting actin polymerization.
- Ethanol inhibited NO generation by inactivating iNOS, promoting Ab survival.
- Alcohol altered cytokine profiles, leading to a dysregulated immune response.
Conclusions:
- Ethanol impairs critical macrophage functions, including phagocytosis and pathogen killing.
- Alcohol-induced immune dysregulation, including reduced NO production and altered cytokine balance, enhances Ab survival and infection severity.
- Ethanol is a significant contributing factor to the exacerbation of Ab infections and CAP in susceptible individuals.
