Wang HJ, Zakhari S, Jung MK. Alcohol, inflammation, and gut-liver-brain interactions in tissue damage and disease development. World J Gastroenterol 2010; 16(11): 1304-1313 [PMID: 20238396 DOI: 10.3748/wjg.v16.i11.1304]
Corresponding Author of This Article
Samir Zakhari, PhD, Director, Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, United States. szakhari@mail.nih.gov
Article-Type of This Article
Topic Highlight
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Mar 21, 2010; 16(11): 1304-1313 Published online Mar 21, 2010. doi: 10.3748/wjg.v16.i11.1304
Alcohol, inflammation, and gut-liver-brain interactions in tissue damage and disease development
H Joe Wang, Samir Zakhari, M Katherine Jung
H Joe Wang, Samir Zakhari, M Katherine Jung, Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, United States
Author contributions: Wang HJ and Jung MK performed the original literature search; all authors contributed to the writing of this manuscript.
Correspondence to: Samir Zakhari, PhD, Director, Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, United States. szakhari@mail.nih.gov
Telephone: +1-301-4430799 Fax: +1-301-5940673
Received: December 21, 2009 Revised: January 21, 2010 Accepted: January 28, 2010 Published online: March 21, 2010
Abstract
Chronic inflammation is often associated with alcohol-related medical conditions. The key inducer of such inflammation, and also the best understood, is gut microflora-derived lipopolysaccharide (LPS). Alcohol can significantly increase the translocation of LPS from the gut. In healthy individuals, the adverse effects of LPS are kept in check by the actions and interactions of multiple organs. The liver plays a central role in detoxifying LPS and producing a balanced cytokine milieu. The central nervous system contributes to anti-inflammatory regulation through neuroimmunoendocrine actions. Chronic alcohol use impairs not only gut and liver functions, but also multi-organ interactions, leading to persistent systemic inflammation and ultimately, to organ damage. The study of these interactions may provide potential new targets for therapeutic intervention.
