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.

Scorpio DG, Von Loewenich FD, Bogdan C, Dumler JS (2005)

Publication Type: Journal article

Publication year: 2005

Journal

Annals of the New York Academy of Sciences New York Academy of Sciences

Book Volume: 1063

Pages Range: 425-428

DOI: 10.1196/annals.1355.077

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.

Authors with CRIS profile

Christian Bogdan

Involved external institutions

Johns Hopkins University (JHU) US United States (USA) (US) Albert-Ludwigs-Universität Freiburg DE Germany (DE)

How to cite

APA:

Scorpio, D.G., Von Loewenich, F.D., Bogdan, C., & Dumler, J.S. (2005). 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. Annals of the New York Academy of Sciences, 1063, 425-428. https://dx.doi.org/10.1196/annals.1355.077

MLA:

Scorpio, Diana G., et al. "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." Annals of the New York Academy of Sciences 1063 (2005): 425-428.

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