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Infection and Immunity, May 2006, p. 2578-2586, Vol. 74, No. 5
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.5.2578-2586.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

The NKG2D-Activating Receptor Mediates Pulmonary Clearance of Pseudomonas aeruginosa

Michael T. Borchers,1,2* Nathaniel L. Harris,1 Scott C. Wesselkamper,1 Shiping Zhang,2 Yi Chen,2 Lisa Young,2,3 and Gee W. Lau2

Department of Environmental Health, Division of Environmental Genetics and Molecular Toxicology,1 Department of Internal Medicine, Division of Pulmonary and Critical Care, University of Cincinnati College of Medicine,2 Division of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 452673

Received 8 November 2005/ Returned for modification 14 December 2005/ Accepted 9 February 2006

The NKG2D-activating receptor is expressed on cytotoxic lymphocytes and interacts with ligands expressed on the surface of cells stressed by pathogenic and nonpathogenic stimuli. In this study, we investigated the physiologic importance of NKG2D receptor-ligand interactions in response to acute pulmonary Pseudomonas aeruginosa infection. P. aeruginosa infection increased the expression of mouse NKG2D ligands (Rae1) in airway epithelial cells and alveolar macrophages in vivo and also increased the cell surface expression of human NKG2D ligands (ULBP2) on airway epithelial cells in vitro. NKG2D receptor blockade with a specific monoclonal antibody inhibited the pulmonary clearance of P. aeruginosa. NKG2D receptor blockade also resulted in decreased production of Th1 cytokines and nitric oxide in the lungs of P. aeruginosa-infected mice. Additionally, NKG2D receptor blockade reduced the epithelial cell sloughing that accompanies P. aeruginosa infection. Macrophage phagocytosis and bronchoalveolar lavage cellularity were not different in P. aeruginosa-infected mice with and without NKG2D receptor blockade. These results demonstrate the importance of NKG2D-mediated immune activation in the clearance of acute bacterial infection and suggest that epithelial cell-lymphocyte interactions mediate pulmonary cytokine production, epithelial cell integrity, and bacterial clearance.

* Corresponding author. Mailing address: Department of Environmental Health, Division of Environmental Genetics, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0056. Phone: (513) 558-6424. Fax: (513) 558-0925. E-mail: michael.borchers{at}uc.edu.

Editor: J. L. Flynn

Infection and Immunity, May 2006, p. 2578-2586, Vol. 74, No. 5
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.5.2578-2586.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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