ArticleAlcoholism, clinical and experimental research2012
Ethanol (EtOH)-induced TGF-β1 and reactive oxygen species production are necessary for EtOH-induced alveolar macrophage dysfunction and induction of alternative activation.
Article in Alcoholism, clinical and experimental research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
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- Pioglitazone Modulates p65-Mediated Mitochondrial Bioenergetics: Implications for Acetaldehyde-Induced HIV Replication in Alveolar Macrophages.Biomolecules · 2025Article
- Alcohol-induced susceptibility to pulmonary bacterial infections: A narrative review.Alcohol, clinical & experimental research · 2025Review
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Liposomal Glutathione Augments Immune Defenses against Respiratory Syncytial Virus in Neonatal Mice Exposed in Utero to Ethanol.Antioxidants (Basel, Switzerland) · 2024Article
- Etiological Changes and Prognosis of Hospitalized Patients with Acute Pancreatitis Over a 15-Year Period.Digestive diseases and sciences · 2024Article
- Pharmacological reversal of post-transcriptional alterations implicated in alcohol-induced alveolar macrophage dysfunction.Alcohol (Fayetteville, N.Y.) · 2023Article
- Innate lymphocytes: Role in alcohol-induced immune dysfunction.Frontiers in immunology · 2022Review
- The Impact of Alcohol Use Disorder on Tuberculosis: A Review of the Epidemiology and Potential Immunologic Mechanisms.Frontiers in immunology · 2022Review
- Hyaladherins May be Implicated in Alcohol-Induced Susceptibility to Bacterial Pneumonia.Frontiers in immunology · 2022Review
- Ethanol promotes alcohol-related colorectal cancer metastasis via the TGF-β/RUNX3/Snail axis by inducing TGF-β1 upregulation and RUNX3 cytoplasmic mislocalization.EBioMedicine · 2019Article
- Role of zinc insufficiency in fetal alveolar macrophage dysfunction and RSV exacerbation associated with fetal ethanol exposure.Alcohol (Fayetteville, N.Y.) · 2019Article
- Alcohol-induced mitochondrial DNA damage promotes injurious crosstalk between alveolar epithelial cells and alveolar macrophages.Alcohol (Fayetteville, N.Y.) · 2019Article
- The involvement of GM-CSF deficiencies in parallel pathways of pulmonary alveolar proteinosis and the alcoholic lung.Alcohol (Fayetteville, N.Y.) · 2019Review
- Dysregulation of Alveolar Macrophage PPARγ, NADPH Oxidases, and TGFβAIDS research and human retroviruses · 2017Article
- Impaired defenses of neonatal mouse alveolar macrophage withPhysiological reports · 2017Article
- Alcohol and lung injury and immunity.Alcohol (Fayetteville, N.Y.) · 2016Review
- Peroxisome Proliferator-Activated Receptor γ Regulates Chronic Alcohol-Induced Alveolar Macrophage Dysfunction.American journal of respiratory cell and molecular biology · 2016Article
- Alcohol abuse and smoking alter inflammatory mediator production by pulmonary and systemic immune cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPrevious studies have shown that chronic ethanol (EtOH) ingestion results in impaired alveolar macrophage function, increased TGF-β(1) production, and decreased antioxidant availability. Similarly, alternative activation (M2 activation) of alveolar macrophages also induces TGF-β(1) production and impairs macrophage function. However, the potential links between EtOH-induced alveolar macrophage derangements, M2 activation, TGF-β(1) production signaling, and oxidant stress have yet to be examined. We hypothesized that EtOH-induced oxidant stress and induction of TGF-β(1) signaling result in alternative activation which subsequently impairs the phagocytic capacity of alveolar macrophages.
methodsPrimary rat alveolar macrophages and the alveolar macrophages cell line NR8383 were treated with 0.08% EtOH ± the antioxidant glutathione (GSH) or a TGF-β(1) neutralizing antibody for 5 days. Outcome measures included TGF-β(1) production, reactive oxygen species (ROS) production, phagocytic capacity, and expression of markers of M2 activation.
resultsChronic EtOH treatment greatly decreased alveolar macrophage phagocytic function, increased ROS production, increased TGF-β(1) , and increased expression of markers of M2 activation. GSH supplementation and inhibition of TGF-β(1) signaling during EtOH treatment prevented these alterations.
conclusionsEtOH treatment increased oxidant stress, TGF-β(1) production, and alternative activation in NR8383 cells. However, GSH supplementation and ablation of TGF-β(1) signaling prevented these effects. This suggested that the EtOH-induced switch to an M2 phenotype was a result of decreased antioxidant availability and increased TGF-β(1) signaling. Preventing EtOH-induced induction of alternative activation may improve alveolar macrophage function in alcoholic subjects and decrease the risk of respiratory infections.
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