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Particulate matter phagocytosis induces tissue factor in differentiating macrophages
M Milano1, P Dongiovanni2, A Artoni3
1Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Milan, Italy.
Journal of Applied Toxicology : JAT
|April 11, 2015
Summary
Airborne particulate matter (PM10) exposure triggers lung macrophages to release tissue factor (TF), increasing blood clot risk. Targeting this mechanism may prevent PM10-related thromboembolic events.
Area of Science:
- Environmental Health
- Immunology
- Hematology
Background:
- Airborne particulate matter (PM10) is linked to thromboembolic events.
- Mechanisms underlying this association require further elucidation.
Purpose of the Study:
- To investigate the impact of PM10 phagocytosis on procoagulant molecule release in human macrophages.
- To assess the effects of PM10 inhalation on tissue factor (TF) expression in rats.
Main Methods:
- Human monocytes differentiated into macrophages were exposed to PM10 in vitro.
- Rats were exposed to PM10 via intratracheal instillation.
- Gene and protein expression of TF and inflammatory markers were analyzed.
Main Results:
- PM10 exposure induced TF mRNA and protein in macrophages, promoting a procoagulant phenotype.
- TF induction required PM10 phagocytosis and was linked to iron retention and oxidative stress.
- Pulmonary PM10 exposure in rats increased local TF expression, elevating circulating TF levels.
Conclusions:
- Phagocytosis of PM10 by lung macrophages induces TF, contributing to thromboembolic risk.
- The anti-inflammatory M2 macrophage phenotype inhibited PM10-induced TF expression.
- Targeting PM10-induced TF may mitigate associated thromboembolic complications.
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