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Published ahead of print on April 22, 2004, doi:10.1164/rccm.200304-478OC

Am. J. Respir. Crit. Care Med., Volume 170, Number 2, July 2004, 188-194

A more recent version of this article appeared on July 15, 2004
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Submitted on April 3, 2003
Accepted on April 16, 2004

Transforming Growth Factor {beta}1 Expression and Activation is Increased in the Alcoholic Rat Lung

Rabih I Bechara1, Lou Ann S Brown2, Jesse Roman1, Pratibha C Joshi1, and David M Guidot1*

1 Section of Pulmonary and Critical Care Medicine, The Atlanta VA Medical Center, Decatur, GA, USA; Division of Pulmonary, Allergy, and Critical Care Medicine, Emory University School of Medicine, Atlanta, GA, USA, 2 Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA

* To whom correspondence should be addressed. E-mail: dguidot{at}emory.edu.

Alcohol abuse increases the incidence of the Acute Respiratory Distress Syndrome (ARDS) more than 3-fold in patients with septic shock. We have shown that chronic ethanol ingestion in a rat model impairs alveolar epithelial barrier function and enhances lung injury during sepsis. We speculated that transforming growth factor beta1 (TGF{beta}1), a pluripotent cytokine implicated in models of epithelial barrier disruption and lung injury, could mediate alveolar epithelial injury in the alcoholic lung. We report that chronic ethanol ingestion (6 wks) in rats increased (P<0.05) TGF{beta}1 mRNA and protein tissue expression, but alone did not induce the release of TGF{beta}1 into the alveolar space. However, during endotoxemia ethanol-fed rats released five-fold more (P<0.05) TGF{beta}1 protein (by ELISA) into the alveolar space than control-fed rats. Further, lung lavage fluid from endotoxemic, ethanol-fed rats had more (P<0.05) biologically active TGF{beta}1 protein, as reflected by anti-TGF{beta}1 antibody-inhibitable induction of permeability in rat alveolar epithelial monolayers in vitro. We conclude that chronic ethanol ingestion increases lung expression of TGF{beta}1 that is released and activated in the alveolar space during endotoxemia where it can disrupt the normally tight epithelial barrier. We speculate that this mechanism could contribute to the increased risk of ARDS in alcoholic patients.
Key words: sepsis, alcoholism, type II cell, epithelium, ARDS




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