Early induction and late abrogation of respiratory burst in A. phagocytophilum - Infected neutrophils

Kyoung Seong Choi, J. Stephen Dumler

Research output: Contribution to journalArticlepeer-review

Abstract

Human granulocytic ehrlichiosis is an emerging tick-borne disease caused by the obligate intracellular pathogen, Anaplasma phagocytophilum. This organism is unique because it survives and propagates in neutrophil vacuoles. During phagocytosis professional phagocytes increase oxygen consumption (respiratory burst) through the activity of NADPH-oxidase, which generates superoxide anion (O2-) and hydrogen peroxide (H2O2). We assayed the ability of A. phagocytophilum-infected neutrophils to generate O2- in response to early infection (0, 3, and 5 hours) by using 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA), a fluorogenic probe commonly used to detect cellular production of reactive oxygen species (ROS). Our flow cytometric analyses showed that cell-free A. phagocytophilum induced respiratory burst 6.9-fold greater than that of LPS, an effect still evident to a lesser degree after 3 h, but absent by 5h. A. phagocytophilum initially induces and then represses respiratory burst in neutrophils. The long-term reduction in respiratory burst activity may be important for survival of A. phagocytophilum and other infectious agents in neutrophils. The effect of this may be to generate a limited functional equivalent of chronic granulomatous disease that predisposes to infections by opportunistic pathogens.

Original languageEnglish (US)
Pages (from-to)488-493
Number of pages6
JournalAnnals of the New York Academy of Sciences
Volume990
DOIs
StatePublished - Jan 1 2003

Keywords

  • Anaplasma phagocytophilum
  • Ehrlichia
  • HGE
  • Respiratory burst

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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