Anaplasma phagocytophilum reduces neutrophil apoptosis in vivo

Helena Scaife1, Zerai Woldehiwet, C Anthony Hart

  • 1School of Biological Sciences, Life Sciences Building, University of Liverpool, Liverpool L69 3BX, United Kingdom.

Infection and Immunity
|March 26, 2003
PubMed

Insights

Sheep neutrophils undergo programmed cell death (apoptosis) naturally. Infection with Anaplasma phagocytophilum delays this process, potentially aiding bacterial survival in these immune cells.

Area of Science:

  • Immunology
  • Cell Biology
  • Veterinary Medicine

Background:

  • Ovine neutrophils undergo spontaneous apoptosis in vitro.
  • Apoptosis is a programmed cell death process crucial for immune regulation.
  • Anaplasma phagocytophilum is an intracellular bacterium that infects neutrophils.

Purpose of the Study:

  • To investigate the effect of Anaplasma phagocytophilum infection on ovine neutrophil apoptosis.
  • To explore the mechanisms influencing neutrophil apoptosis during infection.
  • To understand how altered apoptosis impacts bacterial survival.

Main Methods:

  • Ovine neutrophils were cultured in vitro.
  • Apoptosis was assessed via morphological changes and annexin V binding.
  • Conditioned media from peripheral blood mononuclear cells (PBMC), dexamethasone, sodium butyrate, and actinomycin D were used.
  • Neutrophil function (respiratory burst, chemotaxis) was measured in infected and uninfected sheep.

Main Results:

  • Ovine neutrophils spontaneously underwent apoptosis in vitro.
  • Conditioned PBMC medium partially protected against apoptosis; dexamethasone and sodium butyrate did not.
  • Actinomycin D accelerated neutrophil apoptosis.
  • Neutrophils from Anaplasma phagocytophilum-infected sheep exhibited delayed apoptosis ex vivo.
  • Infection increased neutrophil respiratory burst activity but decreased chemotaxis.

Conclusions:

  • In vivo Anaplasma phagocytophilum infection alters ovine neutrophil apoptosis rates.
  • Delayed apoptosis in infected neutrophils may facilitate bacterial replication.
  • These findings provide insights into the pathogenesis of Anaplasma phagocytophilum infections.