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Effect of a factor released by K562 malignant cells in culture on human neutrophil bactericidal activity

M Amar1, N Amit, C Babin-Chevaye

  • 1Unité 294, Institut National de la Santé et de la Recherche Médical, CHU Xavier Bichat, Paris, France.

Infection and Immunity
|August 1, 1991
PubMed

Insights

A novel inhibitory factor 1 (IF1) from K562 cells impairs neutrophil bactericidal activity against Staphylococcus aureus, particularly when opsonized with complement. This suggests IF1 interferes with complement receptor-mediated functions and oxygen-dependent killing.

Area of Science:

  • Immunology
  • Cell Biology
  • Microbiology

Background:

  • K562 malignant cells release an 8-kDa factor (inhibitory factor 1, IF1) that inhibits neutrophil adherence functions.
  • Previous studies showed IF1 does not affect oxidative burst induced by fMet-Leu-Phe or phorbol ester.

Purpose of the Study:

  • To investigate the effects of IF1 on the bactericidal activity of human polymorphonuclear cells (PMNs) against Staphylococcus aureus.
  • To determine if IF1 affects phagocytosis and chemiluminescence responses of PMNs.

Main Methods:

  • Human PMNs were preincubated with IF1 or control medium.
  • Bactericidal activity against nonopsonized or serum-opsonized S. aureus was assessed by counting surviving bacteria.
  • Phagocytosis and chemiluminescence responses were measured.

Main Results:

  • IF1 diminished PMN bactericidal activity and phagocytosis against complement-opsonized S. aureus.
  • IF1 did not affect killing or phagocytosis of nonopsonized or heat-inactivated serum-opsonized S. aureus.
  • IF1 inhibited PMN chemiluminescence when S. aureus was nonopsonized or complement-opsonized.

Conclusions:

  • IF1 impairs PMN bactericidal activity, likely due to reduced phagocytosis of complement-opsonized bacteria.
  • IF1 interferes with S. aureus stimulation of PMNs via complement receptors.
  • IF1 also affects oxygen-dependent bactericidal activity.

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