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J Infect Dis. 2004 May 15;189(10):1921-5. Epub 2004 Apr 26.

Anaplasma phagocytophilum ligation to toll-like receptor (TLR) 2, but not to TLR4, activates macrophages for nuclear factor-kappa B nuclear translocation.

Author information

1
Division of Medical Microbiology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Abstract

Anaplasma phagocytophilum is an obligate intracellular bacterium that infects neutrophils and causes human anaplasmosis (formerly human granulocytic ehrlichiosis). Interferon (IFN)- gamma causes immunopathology in A. phagocytophilum infection models. Plasma IFN- gamma levels are elevated 4 h after infection in experimentally infected mice, which indicates innate immunity and possible Toll-like receptors (TLRs). The ability of A. phagocytophilum to trigger proinflammatory responses via nuclear factor (NF)- kappa B was tested in TLR2- and TLR4-transfected cell lines and in primary murine macrophages devoid of TLR2 or TLR4. NF- kappa B was activated only through TLR2, which suggests its role in innate immune induction with A. phagocytophilum infections. The role of innate immunity in human anaplasmosis immunopathology requires more study.

PMID:
15122530
DOI:
10.1086/386284
[Indexed for MEDLINE]

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