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.
Scorpio
Diana G
DG
Department of Comparative Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. dscorpio@jhmi.edu
Von Loewenich
Friederike D
FD
Bogdan
Christian
C
Dumler
J Stephen
JS
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