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Clinical and Vaccine Immunology, January 2009, p. 43-48, Vol. 16, No. 1
1071-412X/09/$08.00+0     doi:10.1128/CVI.00282-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Effects of Extracellular ATP on Bovine Lung Endothelial and Epithelial Cell Monolayer Morphologies, Apoptoses, and Permeabilities{triangledown}

David McClenahan,1* Kati Hillenbrand,1 Arvinder Kapur,2 David Carlton,3 and Charles Czuprynski1

Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin,1 Division of Reproductive Endocrinology and Infertility, Department of Obstetrics/Gynecology, School of Medicine, University of Wisconsin-Madison, Madison, Wisconsin,2 Division of Neonatal-Perinatal Medicine, Department of Pediatrics, School of Medicine, Emory University, Atlanta, Georgia3

Received 4 August 2008/ Returned for modification 9 September 2008/ Accepted 27 October 2008

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 pulmonary epithelial (BPE) cells and bovine pulmonary microvascular endothelial cells (BPMEC). Monolayers of BPE cells underwent striking morphological changes when exposed to ATP that included separation of the cells. Neither BPE cells nor BPMEC exhibited increased apoptosis in response to ATP. BPE cell 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 cells, but not BPMEC, 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.

* Corresponding author. Mailing address: University of Northern Iowa, Department of Biology, 1227 W 27th St., Cedar Falls, IA 50614. Phone: (319) 273-2218. Fax: (319) 273-7125. E-mail: david.mcclenahan{at}uni.edu

{triangledown} Published ahead of print on 5 November 2008.

Clinical and Vaccine Immunology, January 2009, p. 43-48, Vol. 16, No. 1
1071-412X/09/$08.00+0     doi:10.1128/CVI.00282-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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