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Effect of Ethanol on Inflammatory Responses

Implications for Pancreatitis
Szabo G.a · Mandrekar P.a · Oak S.a · Mayerle J.b

Author affiliations

aDepartment of Medicine, University of Massachusetts Medical School, Worcester, Mass., USA; bDepartment of Gastroenterology, Endocrinology and Nutrition, Ernst-Moritz-Arndt University, Greifswald, Germany

Corresponding Author

Gyongyi Szabo, MD, PhD

Hepatology and Liver Center, Department of Medicine

University of Massachusetts Medical Center, 364 Plantation Street LRB125

Worcester, MA 01605 (USA)

Tel. +1 508 856 5275 Fax +1 508 856 4770, E-Mail gyongyi.szabo@umassmed.edu

Related Articles for ""

Pancreatology 2007;7:115–123

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Background/Aims: Alcohol use alters inflammatory cell responses. While alcohol has direct effects on pancreatic acinar cells, activation of inflammatory cells is a major component of the pathology of alcoholic pancreatitis. Methods: The effects of acute or chronic alcohol exposure were evaluated in human monocytes on the production of TNFα or IL-10 production, pro-inflammatory gene and nuclear factor-ĸB (NF-ĸB) activation. Results: Moderate, acute alcohol consumption or equivalent doses of alcohol in vitro had anti-inflammatory effects on monocyte activation via inhibition of pro-inflammatory genes and NF-ĸB activation, inhibition of TNFα production and augmentation of the anti-inflammatory cytokine, IL-10. In contrast, acute alcohol treatment augmented NF-ĸB activation and TNFα production and inhibited IL-10 levels in the presence of complex stimulation with combined TLR2 and TLR4 ligands. Prolonged alcohol exposure also resulted in an increase in NF-ĸB and TNFα production in response to TLR4 stimulation with LPS. Conclusion: These results suggest that alcohol can either attenuate or promote inflammatory responses that are critical in pancreatitis. Our results support the hypothesis that both acute alcohol intake in the presence of complex stimuli (such as necrotic cells) and chronic alcohol exposure result in hyper-responsiveness of monocytes to inflammatory signals and may contribute to increased inflammation in pancreatitis.

© 2007 S. Karger AG, Basel and IAP

Article / Publication Details

First-Page Preview
Abstract of Review

Published online: June 21, 2007
Issue release date: July 2007

Number of Print Pages: 9
Number of Figures: 7
Number of Tables: 0

ISSN: 1424-3903 (Print)
eISSN: 1424-3911 (Online)

For additional information: http://www.karger.com/PAN

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