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Related Experiment Videos

Bacterial pathogens modulate an apoptosis differentiation program in human neutrophils.

Scott D Kobayashi1, Kevin R Braughton, Adeline R Whitney

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

Proceedings of the National Academy of Sciences of the United States of America
|September 10, 2003
PubMed
Summary

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Human neutrophils (PMNs) undergo apoptosis to resolve bacterial infections. However, Streptococcus pyogenes accelerates PMN apoptosis and necrosis, potentially aiding pathogen survival and disease progression.

Area of Science:

  • Immunology
  • Molecular Biology
  • Microbiology

Background:

  • Human polymorphonuclear leukocytes (PMNs), or neutrophils, are crucial for innate immunity against bacteria.
  • Neutrophil apoptosis aids in resolving inflammation during bacterial infections.
  • Transcriptional regulation of neutrophil apoptosis during infection remains poorly understood.

Purpose of the Study:

  • To investigate global gene expression changes in human PMNs during phagocytosis of various bacterial pathogens.
  • To identify molecular mechanisms underlying neutrophil apoptosis and its role in resolving bacterial infections.
  • To understand how different bacterial species influence neutrophil apoptosis and immune response.

Main Methods:

  • Global gene expression profiling of human PMNs after phagocytosis of Burkholderia cepacia, Borrelia hermsii, Listeria monocytogenes, Staphylococcus aureus, and Streptococcus pyogenes.

Related Experiment Videos

  • Analysis of gene expression patterns related to apoptosis and innate immune function.
  • Comparative analysis of neutrophil apoptosis kinetics and outcomes induced by different pathogens.

    • Main Results:

    • Phagocytosis of pathogenic bacteria induced a common neutrophil apoptosis differentiation program.
    • Genes for apoptosis effectors were upregulated, while immune receptors were downregulated.
    • Streptococcus pyogenes uniquely altered neutrophil gene expression, downregulating IFN-response genes and accelerating apoptosis followed by necrosis.

    Conclusions:

    • Phagocytosis of bacteria typically induces a PMN apoptosis program that resolves infection.
    • Certain pathogens, like Streptococcus pyogenes, can subvert this program, leading to accelerated apoptosis, necrosis, and potential pathogen survival.
    • These distinct outcomes highlight two fundamental interactions between bacteria and neutrophils: resolution via apoptosis or immune evasion leading to disease.