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.
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.
Department of Comparative Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. dscorpio@jhmi.edu
Diana G
DG
Scorpio
Friederike D
FD
Von Loewenich
Christian
C
Bogdan
J Stephen
JS
Dumler
D041081:Anaplasma phagocytophilum / Q000276:immunology*; D000712:Anaplasmosis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology*; D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D016513:Mice, SCID; D052247:Nitric Oxide Synthase Type II / Q000172:deficiency / Q000235:genetics / Q000378:metabolism; D048069:Tumor Necrosis Factors / Q000378:metabolism
D048069:Tumor Necrosis Factors; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse