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World J Hepatol. May 27, 2011; 3(5): 114-117
Published online May 27, 2011. doi: 10.4254/wjh.v3.i5.114
Pathogenesis of alcoholic hepatitis: Role of inflammatory signaling and oxidative stress
Sarat C Jampana, Rashid Khan
Sarat C Jampana, Departments of Internal Medicine, University of TX Medical Branch, Galveston, TX 77555, United States
Rashid Khan, Departments of Gastroenterology, University of TX Medical Branch, Galveston, TX 77555, United States
Author contributions: Jampana SC drafted and revised the manuscript; Khan R supervised and approved the final version.
Correspondence to: Rashid Khan, MD, Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Texas Medical Branch, 301 Univ. Blvd, Galveston, TX 77555-0764, United States.
Telephone: +1-409-772-1501 Fax: +1-409-772-4789
Received: November 26, 2010
Revised: March 7, 2011
Accepted: March 14, 2011
Published online: May 27, 2011

Inflammatory signaling and oxidative stress are two major components in the pathogenesis of alcoholic hepatitis. Alcohol consumption results in translocation of gut bacteria into the portal system along with lipopolysaccharides that interact with toll-like receptors and results in the production of inflammatory and immunogenic mediators such as tumor necrosis factor-alpha (TNF-α) and interferons. Chronic consumption of alcohol causes priming of this process in which there is enhanced production of cytokines, interferon, interleukins, and TNF-α. Oxidative stress, genetic predisposition, and the unfolded protein response are other contributory mechanisms. Novel therapies aimed at these pathways may prevent, decrease, or delay the complications of alcoholic hepatitis.

Keywords: Alcoholic hepatitis, Lipopolysaccharide, Toll like receptors, Oxidative stress, Endotoxin