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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.
Abstract:
We have previously demonstrated that k562 malignant cells in culture contain and release a low-molecular-mass (8-kDa) factor that inhibits adherence-related functions of neutrophils but does not alter fMet-Leu-Phe- or phorbol ester-induced oxidative burst (M. Amar, N. Amit, T. Pham Huu, S. Chollet-Martin, M.T. Labro, M.A. Gougerot-Pocidalo, and J. Hakim, J. Immunol. 144:4749-4756, 1990). In this study, we investigated the effects of this factor, referred to as inhibitory factor 1 (IF1), on the bactericidal activity of human polymorphonuclear cells (PMNs) on Staphylococcus aureus opsonized in various ways. S. aureus was used either nonopsonized or opsonized with heat-inactivated serum or normal serum containing complement factors. The bactericidal activity of PMNs preincubated with IF1-treated or control medium was examined by counting the surviving bacteria. The ability of IF1-treated PMNs to kill bacteria was diminished when they were opsonized with normal serum. When S. aureus was not opsonized or was opsonized with heat-inactivated serum, the bactericidal activity of IF1-treated PMNs was similar to that of controls. Likewise, the phagocytosis of IF1-treated PMNs was diminished when S. aureus was opsonized with normal serum but was not altered when S. aureus was not opsonized or was opsonized with heat-inactivated serum. These results suggest that the decrease in killing might be due to defective ingestion. The chemiluminescence response of IF1-treated PMNs was inhibited when S. aureus was not opsonized or was opsonized with normal serum. No effect on chemiluminescence was observed when S. aureus was opsonized with heat-inactivated serum. These results suggest that IF1 interferes not only with S. aureus stimulation of PMNs via complement receptors but also with oxygen-dependent bactericidal activity.
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.