ArticlePLoS pathogens2017
Diminished neutrophil extracellular trap (NET) formation is a novel innate immune deficiency induced by acute ethanol exposure in polymicrobial sepsis, which can be rescued by CXCL1.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.
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Who cites it
39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.
- Neutrophil extracellular traps (NETs) and NETosis in alcohol-associated diseases: A systematic review.Alcohol, clinical & experimental research · 2025Pooled it
- Impacts of Curcumin Treatment on Experimental Sepsis: A Systematic Review.Oxidative medicine and cellular longevity · 2023Pooled it
- Neutrophil extracellular traps: A central player in liver diseases.Hepatology communications · 2026Review
- BRD4 modulates antimicrobial defense via non-canonical NRF2 activation in macrophages to confer protection against sepsis.PLoS pathogens · 2026Article
- The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026Review
- Peritoneal neutrophil extracellular traps contribute to septic AKI via peritoneal IL-17A and distant organ CXCL-1/ CXCL-2 pathway in abdominal sepsis.Scientific reports · 2026Article
- Liver as a key organ for systemic antimicrobial defense.Hepatology communications · 2025Review
- Alcohol-induced susceptibility to pulmonary bacterial infections: A narrative review.Alcohol, clinical & experimental research · 2025Review
- Adolescent trauma and alcohol: increased risk for severe head injury and organ dysfunction-insights from the TraumaRegister DGUEuropean journal of trauma and emergency surgery : official publication of the European Trauma Society · 2025Article
- Peritoneal Neutrophil Extracellular Traps contribute to septic AKI via peritoneal IL-17A and distant organ CXCL-1/ CXCL-2 pathway in abdominal sepsis.Research square · 2025Article
- Mitoquinol improves phagocytosis and glycolysis in ethanol-exposed macrophages via HIF-1α-PFKP axis.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The causal relationship between smoking, alcohol consumption, and sepsis: A 2-sample mendelian randomized study.Medicine · 2025Article
- Therapeutic Effects of DNase I on Peripheral and Local Markers of Liver Injury and Neutrophil Extracellular Traps in a Model of Alcohol-Related Liver Disease.International journal of molecular sciences · 2025Article
- Cell-to-cell and organ-to-organ crosstalk in the pathogenesis of alcohol-associated liver disease.eGastroenterology · 2024Article
- Effect of ethanol exposure on innate immune response in sepsis.Journal of leukocyte biology · 2024Review
- The Anti-Thrombotic Effects of PCSK9 Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder.Journal of visualized experiments : JoVE · 2023Article
- Neutrophil degranulation and severely impaired extracellular trap formation at the basis of susceptibility to infections of hemodialysis patients.BMC medicine · 2022Article
- Pleiotropic Effects of PCSK9: Focus on Thrombosis and Haemostasis.Metabolites · 2022Review
- Predicting the Immune Microenvironment and Prognosis with a NETosis-Related lncRNA Signature in Head and Neck Squamous Cell Carcinoma.BioMed research international · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Polymicrobial sepsis is the result of an exaggerated host immune response to bacterial pathogens. Animal models and human studies demonstrate that alcohol intoxication is a key risk factor for sepsis-induced mortality. Multiple chemokines, such as CXCL1, CXCL2 and CXCL5 are critical for neutrophil recruitment and proper function of neutrophils. However, it is not quite clear the mechanisms by which acute alcohol suppresses immune responses and whether alcohol-induced immunosuppression can be rescued by chemokines. Thus, we assessed whether acute ethanol challenge via gavage diminishes antibacterial host defense in a sepsis model using cecal ligation and puncture (CLP) and whether this immunosuppression can be rescued by exogenous CXCL1. We found acute alcohol intoxication augments mortality and enhances bacterial growth in mice following CLP. Ethanol exposure impairs critical antibacterial functions of mouse and human neutrophils including reactive oxygen species production, neutrophil extracellular trap (NET) formation, and NET-mediated killing in response to both Gram-negative (E. coli) and Gram-positive (Staphylococcus aureus) pathogens. As compared with WT (C57Bl/6) mice, CXCL1 knockout mice display early mortality following acute alcohol exposure followed by CLP. Recombinant CXCL1 (rCXCL1) in acute alcohol challenged CLP mice increases survival, enhances bacterial clearance, improves neutrophil recruitment, and enhances NET formation (NETosis). Recombinant CXCL1 (rCXCL1) administration also augments bacterial killing by alcohol-treated and E. coli- and S. aureus-infected neutrophils. Taken together, our data unveils novel mechanisms underlying acute alcohol-induced dysregulation of the immune responses in polymicrobial sepsis, and CXCL1 is a critical mediator to rescue alcohol-induced immune dysregulation in polymicrobial sepsis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.