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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.

Keywords: Chronic alcohol use; Chronic inflammation; Lipopolysaccharides; Pro-inflammatory and anti-inflammatory cytokines; Kupffer cells; Monocytes; Tumor necrosis factor α; Interleukin-10; Neuroendocrine; Hypothalamo-pituitary-adrenal axis; Glucocorticoid