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Procoagulant (thromboplastin) activity in human bronchoalveolar lavage fluids is derived from alveolar macrophages

T Lyberg1, B Nakstad, O Hetland

  • 1Department of Surgery, Ullevål University Hospital, Oslo, Norway.

Insights

Lung macrophages release tissue factor on microvesicles, contributing to fibrin deposition and potentially pulmonary fibrosis in inflammatory lung diseases.

Area of Science:

  • Pulmonary Medicine
  • Hematology
  • Cell Biology

Background:

  • Fibrin deposition in lung tissues is characteristic of inflammatory pulmonary diseases.
  • Monocyte/macrophage cells are key sources of procoagulant activity in inflammation.

Purpose of the Study:

  • To investigate the presence and nature of procoagulant activities in human lung alveolar macrophages (LAM) and bronchoalveolar lavage fluid (BALF).
  • To determine the cellular origin and biochemical identity of the procoagulant factors.

Main Methods:

  • Analysis of procoagulant activity in LAM and BALF.
  • Ultracentrifugation of BALF to isolate membrane vesicles.
  • Electron microscopy and enzyme marker analysis of BALF sediment.
  • Macrophage membrane marker analysis to identify vesicle origin.
  • Biochemical characterization including phospholipase C sensitivity and antibody neutralization.

Main Results:

  • Both LAM and BALF exhibited significant procoagulant activities.
  • The procoagulant in BALF was associated with membrane vesicles derived partly from LAM.
  • The procoagulant activity was identified as thromboplastin (tissue factor) or tissue factor-factor VII complexes.

Conclusions:

  • Alveolar macrophages and their derived microvesicles containing thromboplastin contribute to fibrin deposition in the lungs.
  • This process may play a role in the development of pulmonary fibrosis.

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