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Frontline: Control of Anaplasma phagocytophilum , an obligate intracellular pathogen, in the absence of inducible nitric oxide synthase, phagocyte NADPH oxidase, tumor necrosis factor, Toll‐like receptor (TLR)2 and TLR4, or the TLR adaptor molecule MyD88
Author(s) -
von Loewenich Friederike D.,
Scorpio Diana G.,
Reischl Udo,
Dumler J. Stephen,
Bogdan Christian
Publication year - 2004
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.200425029
Subject(s) - biology , anaplasma phagocytophilum , phagocyte , microbiology and biotechnology , tumor necrosis factor alpha , nitric oxide synthase , intracellular parasite , toll like receptor , nadph oxidase , immunology , innate immune system , nitric oxide , phagocytosis , immune system , antibody , reactive oxygen species , borrelia burgdorferi , endocrinology
Anaplasma phagocytophilum is an obligate intracellular bacterium that is related to rickettsial organisms and replicates in the hostile environment of neutrophils. Previous studies with SCID mice suggested that T and/or B cells are required for its control in vivo. Here, we used mice deficient for Toll-like receptor (TLR)2 and TLR4, MyD88, tumor necrosis factor, inducible nitric oxide synthase, or phagocyte NADPH oxidase (gp91(phox-/-)) to define the pathways that are critical for the recognition and the killing of this pathogen. Whereas SCID mice developed a 60-fold higher bacterial load in the blood compared to wild-type mice and succumbed to infection, all other gene-deficient mouse strains were fully capable in overcoming a systemic infection with A. phagocytophilum. From these data we conclude that effector mechanisms that are crucial to the defense against numerous other intracellular pathogens are dispensable for the control of A. phagocytophilum.