ArticleAlcoholism, clinical and experimental research2013
Chronic alcohol induces M2 polarization enhancing pulmonary disease caused by exposure to particulate air pollution.
Article in Alcoholism, clinical and experimental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Sarcopenia and Frailty in COPD: Mechanisms, Relationship with Malnutrition and Potential Therapeutic Interventions.Nutrients · 2026Review
- Alcohol consumption and cancer progression: Mechanistic insights, immune dysregulation, and public health implications.Translational oncology · 2026Review
- The alcohol exposome.Alcohol (Fayetteville, N.Y.) · 2025Review
- Predominantly Pro-Inflammatory Phenotype with Mixed M1/M2 Polarization of Peripheral Blood Classical Monocytes and Monocyte-Derived Macrophages among Patients with Excessive Ethanol Intake.Antioxidants (Basel, Switzerland) · 2023Article
- Developmental Hazard of Environmentally Persistent Free Radicals and Protective Effect of TEMPOL in Zebrafish Model.Toxics · 2021Article
- Alcohol induces TGFβ1 via downregulation of miR-1946a in murine lung fibroblast.Scientific reports · 2020Article
- The Role and Potential Pathogenic Mechanism of Particulate Matter in Childhood Asthma: A Review and Perspective.Journal of immunology research · 2020Review
- The involvement of GM-CSF deficiencies in parallel pathways of pulmonary alveolar proteinosis and the alcoholic lung.Alcohol (Fayetteville, N.Y.) · 2019Review
- Pre- and postnatal exposure of mice to concentrated urban PMEnvironmental pollution (Barking, Essex : 1987) · 2018Article
- Macrophage polarization and function: new prospects for fibrotic disease.Immunology and cell biology · 2017Review
- Alcohol abuse and smoking alter inflammatory mediator production by pulmonary and systemic immune cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Alveolar macrophage inflammatory mediator expression is elevated in the setting of alcohol use disorders.Alcohol (Fayetteville, N.Y.) · 2016Article
- Chronic alcohol ingestion in rats alters lung metabolism, promotes lipid accumulation, and impairs alveolar macrophage functions.American journal of respiratory cell and molecular biology · 2014Article
- Exposure to combustion generated environmentally persistent free radicals enhances severity of influenza virus infection.Particle and fibre toxicology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic alcohol consumption causes persistent oxidative stress in the lung, leading to impaired alveolar macrophage (AM) function and impaired immune responses. AMs play a critical role in protecting the lung from particulate matter (PM) inhalation by removing particulates from the airway and secreting factors which mediate airway repair. We hypothesized AM dysfunction caused by chronic alcohol consumption increases the severity of injury caused by PM inhalation.
methodsAge- and sex-matched C57BL/6 mice were fed the Lieber-DeCarli liquid diet containing either alcohol or an isocaloric substitution (control diet) for 8 weeks. Mice from both diet groups were exposed to combustion-derived PM (CDPM) for the final 2 weeks. AM number, maturation, and polarization status were assessed by flow cytometry. Noninvasive and invasive strategies were used to assess pulmonary function and correlated with histomorphological assessments of airway structure and matrix deposition.
resultsCo-exposure to alcohol and CDPM decreased AM number and maturation status (CD11c expression), while increasing markers of M2 activation (interleukin [IL]-4Rα, Ym1, Fizz1 expression, and IL-10 and transforming growth factor [TGF]-β production). Changes in AM function were accompanied by decreased airway compliance and increased elastance. Altered lung function was attributable to elevated collagen content localized to the small airways and loss of alveolar integrity. Intranasal administration of neutralizing antibody to TGF-β during the CDPM exposure period improved changes in airway compliance and elastance, while reducing collagen content caused by co-exposure.
conclusionsCombustion-derived PM inhalation causes enhanced disease severity in the alcoholic lung by stimulating the release of latent TGF-β stores in AMs. The combinatorial effect of elevated TGF-β, M2 polarization of AMs, and increased oxidative stress impairs pulmonary function by increasing airway collagen content and compromising alveolar integrity.
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