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.

Diana G. Scorpio, Friederike D. Von Loewenich, Christian Bogdan, J. Stephen Dumler

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Pages (from-to)425-428
Number of pages4
JournalAnnals of the New York Academy of Sciences
Volume1063
DOIs
StatePublished - Dec 2005

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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