HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Szabo, G. Articles by Pruett, S. B. Search for Related Content PubMed PubMed Citation Articles by Szabo, G. Articles by Pruett, S. B. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Compound via MeSH Substance via MeSH Hazardous Substances DB ETHANOL

TLR4, Ethanol, and Lipid Rafts: A New Mechanism of Ethanol Action with Implications for other Receptor-Mediated Effects

Gyongyi Szabo^1,2,*, Angela Dolganiuc^*, Qun Dai and Stephen B. Pruett^1,

^* University of Massachusetts Medical School, Worcester, MA 01605; and Louisiana State University Health Sciences Center, Shreveport, LA 71130

Ethanol (EtOH) is the most widely abused substance in the United States, and it contributes to well-documented harmful (at high dosages) and beneficial (at low dosages) changes in inflammatory and immune responses. Lipid rafts have been implicated in the regulation and activation of several important receptor complexes in the immune system, including the TLR4 complex. Many questions remain about the precise mechanisms by which rafts regulate the assembly of these receptor complexes. Results summarized in this review indicate that EtOH acts by altering the LPS-induced redistribution of components of the TLR4 complex within the lipid raft and that this is related to changes in actin cytoskeleton rearrangement, receptor clustering, and subsequent signaling. EtOH provides an example of an immunomodulatory drug that acts at least in part by modifying lipid rafts, and it could represent a model to probe the relationships between rafts, receptor complexes, and signaling.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ G.S. and S.B.P. contributed equally.

² Address correspondence and reprint requests to Dr. Gyongyi Szabo, Director of Hepatology and Liver Center, Department of Medicine, University of Massachusetts Medical Center, 364 Plantation Street LRB125, Worcester, MA 01605. E-mail address: gyongyi.szabo{at}umassmed.edu

³ Abbreviations used in this paper: EtOH, ethanol; GABA, -aminobutyric acid; TIR, Toll/IL-1 receptor.

This article has been cited by other articles:

				J. E. Baenziger, S. E. Ryan, M. M. Goodreid, N. Q. Vuong, R. M. Sturgeon, and C. J. B. daCosta Lipid Composition Alters Drug Action at the Nicotinic Acetylcholine Receptor Mol. Pharmacol., March 1, 2008; 73(3): 880 - 890. [Abstract] [Full Text] [PDF]