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Clinical and Vaccine Immunology, July 2006, p. 806-809, Vol. 13, No. 7
1071-412X/06/$08.00+0 doi:10.1128/CVI.00092-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Department of Molecular and Comparative Pathobiology,1 Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland,2 Institute of Medical Microbiology and Hygiene, University of Freiburg, Freiburg, Germany,3 Department of Pathology, University of Freiburg, Freiburg, Germany4
Received 8 March 2006/ Returned for modification 14 April 2006/ Accepted 5 May 2006
In mice, Anaplasma phagocytophilum control is independent of phagocyte oxidase (phox), inducible NO synthase (NOS2), tumor necrosis factor (TNF), and MyD88 Toll-like receptor signaling. We show that despite evasion of these host responses, phox, NOS2, TNF, and MyD88 are activated and contribute to inflammation and hepatic injury more than A. phagocytophilum itself.
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