ArticleAlcoholism, clinical and experimental research2009
Alcohol primes the airway for increased interleukin-13 signaling.
Article in Alcoholism, clinical and experimental research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Chronic alcohol use primes bronchial cells for altered inflammatory response and barrier dysfunction during SARS-CoV-2 infection.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Primary graft dysfunction following lung transplantation: From pathogenesis to future frontiers.World journal of transplantation · 2023Review
- Inflammatory Biomarkers, Microbiome, Depression, and Executive Dysfunction in Alcohol Users.International journal of environmental research and public health · 2020Article
- Article
- Review
- Krüppel-like factor 4 is a transcriptional regulator of M1/M2 macrophage polarization in alcoholic liver disease.Journal of leukocyte biology · 2015Article
- Junctional adhesion molecule A promotes epithelial tight junction assembly to augment lung barrier function.The American journal of pathology · 2015Article
- 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
- Heavy alcohol use in lung donors increases the risk for primary graft dysfunction.Alcoholism, clinical and experimental research · 2014Article
- Chronic alcohol ingestion and predisposition to lung "cirrhosis".Alcoholism, clinical and experimental research · 2014Article
- Alcohol ingestion disrupts alveolar epithelial barrier function by activation of macrophage-derived transforming growth factor beta1.Respiratory research · 2013Article
- Ethanol (EtOH)-induced TGF-β1 and reactive oxygen species production are necessary for EtOH-induced alveolar macrophage dysfunction and induction of alternative activation.Alcoholism, clinical and experimental research · 2012Article
- Expression of IL-4/IL-13 receptors in differentiating human airway epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2010Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundUsing an experimental model of airway fibrosis following lung transplantation, we recently showed that chronic alcohol ingestion by donor rats amplifies airway fibrosis in the recipient. Associated with alcohol-mediated amplification of airway fibrosis is increased transforming growth factor beta-1(TGFbeta(1)) and alpha-smooth muscle actin expression. Other studies have shown that interleukin-13 (IL-13) modulates TGFbeta(1) signaling during experimentally-induced airway fibrosis. Therefore, we hypothesized that IL-13 is a component of alcohol-mediated amplification of pro-fibrotic mediators in the alcoholic lung.
methodsTo test this hypothesis, we analyzed tracheal epithelial cells and type II alveolar cells from control- or alcohol-fed rats, alcohol-treated mouse lung fibroblasts, and human bronchial epithelial cells in vitro for expression of various components of the IL-13 signaling pathway. Signaling via the IL-13 pathway was assessed by measuring levels of phosphorylated signal transducers and activators of transcription-6 (STAT6). In addition, we performed heterotopic tracheal transplantation using control-fed and alcohol-fed donor rats and analyzed tracheal allografts for expression of components of the IL-13 signaling pathway by RT-PCR and immunocytochemical analyses.
resultsInterleukin-13 expression was detected in type II alveolar epithelial cells and human bronchial epithelial cells, but not in lung fibroblasts. IL-13 expression was decreased in whole lung and type II cells in response to alcohol exposure. In all cell types analyzed, expression of IL-13 signaling receptor (IL-13R alpha(1)) mRNA was markedly increased. In contrast, mRNA and protein expression of the IL-13 decoy receptor (IL-13R alpha(2)) were decreased in all cells analyzed. Exposure to alcohol also increased STAT6 phosphorylation in response to IL-13 and lipopolysaccharide.
conclusionsData from multiple cell types in the pulmonary system suggest that IL-13 and its receptors play a role in alcohol-mediated activation of pro-fibrotic pathways. Taken together, these data suggest that alcohol primes the airway for increased IL-13 signaling and subsequent tissue remodeling upon injury such as transplantation.
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