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Ann N Y Acad Sci. 2005 Dec;1063:425-8.

Innate immune tissue injury and murine HGA: tissue injury in the murine model of granulocytic anaplasmosis relates to host innate immune response and not pathogen load.

Author information

1
Department of Comparative Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. dscorpio@jhmi.edu

Abstract

Anaplasma phagocytophilum is an obligate intracellular tick-borne bacterium that propagates within neutrophils and causes human and animal granulocytic anaplasmosis (HGA). In the murine model of HGA, host immune response plays a more important role in histopathologic lesions than does pathogen load. We examined the role of CYBB, NOS2, and TNFalpha as effectors of innate immune-related injury. Our hypothesis is that the innate immune response to A. phagocytophilum results in inflammatory histopathology, but does not control the pathogen.

PMID:
16481553
DOI:
10.1196/annals.1355.077
[Indexed for MEDLINE]

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