Ethanol (EtOH)-Induced TGF-β1 and Reactive Oxygen Species Production Are Necessary for EtOH-Induced Alveolar Macrophage Dysfunction and Induction of Alternative Activation

• Published in: Alcoholism, clinical and experimental research Vol. 36; no. 11; pp. 1952 - 1962
• Main Authors: Brown, Sheena D., Brown, Lou Ann S.
• Format: Journal Article
• Language: English
• Published: Hoboken, NJ Blackwell Publishing Ltd 01.11.2012; Wiley
• Subjects: Alcoholism and acute alcohol poisoning; Alternative Activation; Animals; Biological and medical sciences; Cell Line; Ethanol - toxicity; Glutathione; Macrophage; Macrophage Activation - drug effects; Macrophage Activation - physiology; Macrophages, Alveolar - drug effects; Macrophages, Alveolar - metabolism; Macrophages, Alveolar - pathology; Male; Medical sciences; Oxidative Stress; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species - metabolism; TGF-β1; Toxicology; Transforming Growth Factor beta1 - biosynthesis; Transforming Growth Factor beta1 - physiology; Oxidative stress; Reactive oxygen species; Ethanol; Induction; Activation; Biosynthesis; Alcoholic beverage; Dysfunction; TGF-β; Transforming growth factor β1; Alternative Activation; Glutathione; Macrophage

Background Previous studies have shown that chronic ethanol (EtOH) ingestion results in impaired alveolar macrophage function, increased TGF‐β1 production, and decreased antioxidant availability. Similarly, alternative activation (M2 activation) of alveolar macrophages also induces TGF‐β1 production...