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Modulation of alveolar macrophage leukotriene B4 released by complement component C5
R A Robbins1, G L Gossman, L A Allington
1Research Service, Omaha Veterans Administration Medical Center, NE.
The Journal of Laboratory and Clinical Medicine
|April 1, 1990
Summary
Guinea pig alveolar macrophages release neutrophil chemotactic activity dependent on complement C5. Human alveolar macrophages showed that cell surface C5 modulates leukotriene B4 (LTB4) release, a potent chemotactic factor.
Area of Science:
- Immunology
- Cell Biology
- Respiratory Medicine
Background:
- Neutrophil chemotactic activity is crucial for immune responses.
- Alveolar macrophages (AMs) release neutrophil chemoattractants.
- The fifth component of complement (C5) on cell surfaces influences macrophage functions.
Purpose of the Study:
- To investigate the role of cell surface C5 in modulating leukotriene B4 (LTB4) release by human AMs.
- To determine if C5 influences the release of LTB4, a potent chemotactic factor.
- To assess the impact of C5 on the neutrophil chemotactic activity of AM supernatants.
Main Methods:
- Human AMs were obtained via bronchoalveolar lavage from 12 subjects.
- AMs were cultured with stimuli (opsonized zymosan, immune complexes, lipopolysaccharide) and anti-C5 Fab' antibodies.
- Leukotriene B4 (LTB4) levels were quantified using radioimmunoassay, and neutrophil chemotactic activity was assessed.
Main Results:
- Stimuli significantly increased LTB4 release from AMs compared to media alone.
- Anti-C5 Fab' antibodies significantly inhibited LTB4 release induced by all tested stimuli.
- Anti-C5 Fab' antibodies also significantly decreased the neutrophil chemotactic activity of stimulated AM supernatants.
Conclusions:
- The release of LTB4 by human alveolar macrophages is dependent on cell surface C5.
- C5 plays a modulatory role in the inflammatory response mediated by AMs.
- Targeting C5 may represent a therapeutic strategy to control macrophage-driven inflammation.