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Procoagulant activities in human alveolar macrophages
European Journal of Respiratory Diseases
|November 1, 1987
Summary
Lung alveolar macrophages (LAM) initiate blood clotting by releasing procoagulant microvesicles. These findings suggest LAM and their shed vesicles contribute to fibrin deposition in chronic lung inflammation.
Area of Science:
- Pulmonary Medicine
- Hematology
- Cell Biology
Background:
- Fibrin and tissue macrophages coexist in chronic lung inflammation.
- Human lung alveolar macrophages (LAM) can initiate coagulation via procoagulant factors.
Purpose of the Study:
- Identify LAM procoagulants.
- Investigate LAM procoagulant activity and vesicle release.
Main Methods:
- LAM lavage from healthy donors.
- Density gradient centrifugation to separate LAM subpopulations.
- Characterization of procoagulant factors and microvesicles.
Main Results:
- LAM procoagulants identified as thromboplastin or a factor X activator.
- Low-density LAM subpopulations released procoagulant microvesicles.
- LAM showed no inducible thromboplastin synthesis unlike monocytes.
Conclusions:
- LAM and their shed microvesicles contribute to lung fibrin deposition.
- Procoagulant activity is linked to LAM density and vesicle shedding.