Anaplasma phagocytophilum ligation to Toll-Like Receptor (TLR) 2, but not to TLR4, activates macrophages for nuclear factor-κB nuclear translocation

Kyoung Seong Choi, Diana G. Scorpio, J. Stephen Dumler

Research output: Contribution to journalArticlepeer-review

Abstract

Anaplasma phagocytophilum is an obligate intracellular bacterium that infects neutrophils and causes human anaplasmosis (formerly human granulocytic ehrlichiosis). Interferon (IFN)-γ causes immunopathology in A. phagocytophilum infection models. Plasma IFN-γ 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)-κB was tested in TLR2- and TLR4-transfected cell lines and in primary murine macrophages devoid of TLR2 or TLR4. NF-κB 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.

Original languageEnglish (US)
Pages (from-to)1921-1925
Number of pages5
JournalJournal of Infectious Diseases
Volume189
Issue number10
DOIs
StatePublished - May 15 2004

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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