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Human alveolar macrophages release a factor that inhibits phagocyte function.
Y Sibille1, W W Merrill, G P Naegel
1Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510.
American Journal of Respiratory Cell and Molecular Biology
|November 1, 1989
Summary
Human alveolar macrophages release a novel inhibitory factor that modulates neutrophil and monocyte movement and respiratory burst. This factor, a low-molecular-weight nonpolar substance, affects chemotaxis without blocking receptor binding.
Area of Science:
- Immunology
- Cell Biology
- Respiratory Medicine
Background:
- Human alveolar macrophages play a role in lung immunity.
- These macrophages can release factors influencing neutrophil behavior.
Purpose of the Study:
- To investigate the properties and effects of a newly identified inhibitor released by human alveolar macrophages.
- To determine the impact of this inhibitor on polymorphonuclear neutrophil (PMN) and monocyte functions.
Main Methods:
- In vitro culture of human alveolar macrophages.
- Collection and separation of culture supernatants using HPLC.
- Assays for random migration and chemotaxis of PMNs and monocytes.
- Measurement of superoxide release by PMNs.
Main Results:
- Alveolar macrophages release a non-cytotoxic, low-molecular-weight inhibitor (<1,000 D).
- The inhibitor significantly reduces PMN chemotaxis induced by FMLP, C5a, and LTB4, and also affects monocyte chemotaxis.
- It diminishes PMA and FMLP-induced superoxide release by PMNs but does not affect random migration.
- The inhibitor is partially heat labile, sensitive to aminopeptidase M, and nonpolar.
Conclusions:
- Human alveolar macrophages produce a factor that inhibits neutrophil and monocyte chemotaxis and PMN respiratory burst.
- This inhibitor modulates immune cell function in the alveolar space.
- The inhibitor does not interfere with chemoattractant receptor binding on PMNs.