We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
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.
- Authors
SCORPIO, DIANA G.; LOEWENICH, FRIEDERIKE D.; BOGDAN, CHRISTIAN; DUMLER, J STEPHEN
- 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 TNF 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.
- Subjects
ANAPLASMOSIS; CHRONIC granulomatous disease; IMMUNE system; HISTOPATHOLOGY; PHAGOCYTE metabolism
- Publication
Annals of the New York Academy of Sciences, 2005, Vol 1063, Issue 1, p425
- ISSN
0077-8923
- Publication type
Article
- DOI
10.1196/annals.1355.077