CVI Accepts, published online ahead of print on 5 November 2008

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Clin. Vaccine Immunol. doi:10.1128/CVI.00282-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Effects of extracellular ATP on bovine lung endothelial and epithelial cell monolayer morphology, cell death, and permeability

David McClenahan^*, Kati Hillenbrand, Arvinder Kapur, David Carlton, and Charles Czuprynski

Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin—Madison, Madison, WI; Division of Reproductive Endocrinology and Infertility, Department of Obstetrics/Gynecology, School of Medicine, University of Wisconsin—Madison, Madison, WI; Division of Neonatal-Perinatal Medicine, Department of Pediatrics, School of Medicine, Emory University, Atlanta, GA

^* To whom correspondence should be addressed. Email: david.mcclenahan{at}uni.edu.

Pneumonia in cattle is an important disease both economically and in terms of animal welfare. Recent evidence in other species has shown ATP to be an important modulator of inflammation in the lung, where it is released by activated alveolar macrophages and damaged lung cells. Whether ATP serves a similar process during infection in the bovine lung, is unknown. In the present study, we examined the effects of ATP treatment on the morphology, apoptosis, and permeability of bovine lung epithelial (BPE) and microvascular endothelial cells (BPMEC). Monolayers of BPE cells underwent striking morphologic changes when exposed to ATP that included separation of the cells. Neither BPE nor BPMEC cells exhibited increased apoptosis in response to ATP. BPE and BPMEC monolayers displayed virtually identical increases in permeability when exposed to ATP, with a 50% change occurring within the first hour of exposure. Both cell types contained mRNA for the P2X₇ receptor, a known receptor for ATP. In BPE, but not BPMEC cells, the change in permeability in response to ATP was reversed by the addition of a P2X₇ receptor antagonist. If similar permeability changes occur in vivo, they could be a factor in vascular leakage into lung airspaces during pneumonia.