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Human alveolar macrophages prevent apoptosis in polymorphonuclear leukocytes
J P Herlihy1, M W Vermeulen, C A Hales
1Pulmonary and Critical Care Unit, Massachusetts General Hospital, Boston, USA.
The American Journal of Physiology
|November 1, 1996
Summary
Alveolar macrophages (AM) release factors like TNF-alpha and GM-CSF that delay programmed cell death (apoptosis) in neutrophils (PMN). Activated AM can significantly suppress PMN apoptosis, aiding lung defense.
Area of Science:
- Immunology
- Cell Biology
- Pulmonary Medicine
Background:
- Polymorphonuclear leukocytes (PMN) are crucial for lung defense against pathogens and injury.
- PMN normally undergo rapid apoptosis and lysis, limiting their functional lifespan.
- Alveolar macrophages (AM) are hypothesized to provide signals that prevent PMN apoptosis.
Purpose of the Study:
- To investigate whether alveolar macrophages (AM) can prevent polymorphonuclear leukocyte (PMN) apoptosis.
- To identify factors produced by AM that influence PMN survival.
Main Methods:
- AM were isolated from healthy volunteers via bronchoalveolar lavage.
- AM-conditioned media (AM-CM) were generated.
- Freshly isolated PMN were cultured in AM-CM or unconditioned media (UM) for 48 hours.
- Apoptosis and survival rates of PMN were assessed.
Main Results:
- AM-CM from most subjects modestly delayed PMN apoptosis compared to UM.
- In one subject with urticaria, AM-CM profoundly inhibited PMN apoptosis and enhanced survival.
- Tumor necrosis factor-alpha (TNF-alpha) and granulocyte/macrophage colony-stimulating factor (GM-CSF) were identified as contributing factors.
Conclusions:
- AM produce TNF-alpha, which delays PMN apoptosis.
- In certain conditions, like allergic reactions, AM can produce GM-CSF, leading to a more profound suppression of PMN apoptosis.
- Activated AM play a significant role in regulating PMN lifespan and function in the lungs.