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Related Experiment Videos

An apoptosis differentiation programme in human polymorphonuclear leucocytes.

S D Kobayashi1, F R Deleo

  • 1Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South 4th Street, Hamilton, MT 59840, USA.

Biochemical Society Transactions
|May 26, 2004
PubMed
Summary
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Human neutrophils initiate innate immunity but their inflammatory response termination is unclear. Genomics revealed an apoptosis differentiation program regulating neutrophil maturation and resolving bacterial infections.

Area of Science:

  • Immunology
  • Molecular Biology
  • Microbiology

Background:

  • Human neutrophils (polymorphonuclear leukocytes) are crucial for innate immunity against bacterial pathogens and acute inflammation.
  • The molecular mechanisms underlying the resolution of inflammation during human bacterial infections remain largely undefined.

Purpose of the Study:

  • To investigate the molecular basis for the termination of neutrophil-mediated inflammation during bacterial infection.
  • To gain insight into processes facilitating the resolution of neutrophil-mediated inflammation and bacterial infection using genomics strategies.

Main Methods:

  • Genomics strategies were employed to analyze gene expression changes in human neutrophils.
  • Studies focused on post-phagocytic processes and the role of reactive oxygen species.

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Main Results:

  • Global changes in neutrophil gene expression after phagocytosis constitute an apoptosis differentiation program.
  • This program represents a transcription-regulated final stage of neutrophil maturation.
  • The apoptosis differentiation program influences neutrophil cell fate and pro-inflammatory activity, modulated by reactive oxygen species.

Conclusions:

  • A global model of host cell-pathogen interaction is established.
  • This model provides fundamental insights into the resolution of human bacterial infections.
  • The apoptosis differentiation program is a key mechanism in resolving neutrophil-mediated inflammation.