NDLI: NKG2D is critical for NK cell activation in host defense against Pseudomonas aeruginosa respiratory infection.

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NKG2D is critical for NK cell activation in host defense against Pseudomonas aeruginosa respiratory infection.

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NKG2D is critical for NK cell activation in host defense against Pseudomonas aeruginosa respiratory infection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Eppert, Bryan L. Lau, Gee W. Borchers, Michael T. Wesselkamper, Scott C. Motz, Gregory T. Hassett, Daniel J.
Description	Country affiliation: United States Author Affiliation: Wesselkamper SC ( Department of Environmental Health, Division of Environmental Genetics and Molecular Toxicology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.)
Abstract	Pseudomonas aeruginosa is a major cause of nosocomial respiratory infections. The eradication of P. aeruginosa from the lung involves the orchestrated actions of the pulmonary epithelium and both resident and recruited immune cells. The NKG2D receptor is constitutively expressed on the surface of circulating and tissue-resident NK cells (and other cytotoxic lymphocytes), and is capable of controlling NK cell activation and production of cytokines, such as IFN-gamma via interactions with ligands expressed on the surface of stressed cells. Previously, we demonstrated that NKG2D mediates pulmonary clearance of P. aeruginosa. In the present study, we investigated the cellular and molecular mechanisms of NKG2D-mediated clearance of P. aeruginosa using a novel transgenic mouse model of doxycycline-inducible conditional expression of NKG2D ligands (retinoic acid early transcript 1, alpha) in pulmonary epithelial cells. NKG2D ligand expression in this model increased pulmonary clearance, cellular phagocytosis, and survival following P. aeruginosa respiratory infection. Additionally, NK cell sensitivity to ex vivo LPS stimulation was greater in lung cells isolated from naive transgenic mice administered doxycycline. We also showed that NK cells are the primary source of lymphocyte-derived IFN-gamma in response to P. aeruginosa respiratory infection. Significantly, we demonstrated that NKG2D is critical to the nonredundant IFN-gamma production by pulmonary NK cells following acute P. aeruginosa infection. These results represent the principal report of NKG2D-mediated activation of lung NK cells following respiratory infection with an opportunistic pathogen and further establish the importance of NKG2D in the host response against P. aeruginosa respiratory infection.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	8
Volume Number	181
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2008-10-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Killer Cells, Natural Immunology Lymphocyte Activation Pseudomonas Infections Pseudomonas Aeruginosa Receptors, Immunologic Respiratory Tract Infections Animals Gene Expression Genetics Interferon-gamma Lipopolysaccharides Pharmacology Lung Membrane Proteins Mice Mice, Transgenic Nk Cell Lectin-like Receptor Subfamily K Opportunistic Infections Receptors, Natural Killer Cell Respiratory Mucosa Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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