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Pleural mesothelial cells modulate polymorphonuclear leukocyte apoptosis in empyema
Najmunnisa Nasreen1, Kamal A Mohammed, Kerry L Sanders
1Division of Pulmonary and Critical Care Medicine, Veterans' Affairs Medical Center, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Journal of Clinical Immunology
|March 21, 2003
Summary
In bacterial empyema, Staphylococcus aureus-activated cells release granulocyte colony-stimulating factor (GM-CSF), delaying polymorphonuclear leukocyte (PMN) apoptosis. This extends PMN lifespan, crucial for fighting infection.
Area of Science:
- Immunology
- Cell Biology
- Infectious Diseases
Background:
- Polymorphonuclear leukocytes (PMN) are key in bacterial empyema defense.
- Pleural fluids (PF) from empyema (EMP) patients show elevated granulocyte colony-stimulating factor (GM-CSF).
Purpose of the Study:
- To investigate the role of GM-CSF in PMN apoptosis in empyema.
- To understand how Staphylococcus aureus-stimulated cells influence PMN lifespan.
Main Methods:
- Incubation of PMN in empyema PF and control PF.
- Stimulation of PMN with Staphylococcus aureus.
- Analysis of apoptosis markers, gene expression (Bcl-xL, Bak), and caspase activity.
- Immunodepletion of GM-CSF.
Main Results:
- Empyema PF and Staphylococcus aureus-stimulated PMN supernatant (SPMC-CM) significantly reduced PMN apoptosis.
- SPMC-CM upregulated anti-apoptotic Bcl-xL and downregulated pro-apoptotic Bak.
- GM-CSF depletion increased PMN apoptosis, indicating its crucial role.
Conclusions:
- GM-CSF released by S. aureus-activated cells delays PMN apoptosis in empyema.
- This modulation of apoptosis extends PMN lifespan, aiding bacterial defense.