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Generation of Lymphocytic Microparticles and Detection of their Proapoptotic Effect on Airway Epithelial Cells
Published on: February 20, 2015
Platelet-derived microparticles induce polymorphonuclear leukocyte-mediated damage of human pulmonary microvascular
Ru Feng Xie1, Ping Hu2, Zhi Cheng Wang3
1Shanghai Blood Center, Shanghai, China.
Background:
Platelets (PLTs) stored at 22°C accumulate microparticles and biologic response modifiers (BRMs) that induce inflammatory reactions in transfusion recipients. However, soluble BRMs are fully diluted in the recipient's blood circulation. The mechanisms by which BRMs exert their effects have not been elucidated. The objectives of this study were to determine the effect of PLT microparticles (PMPs) on polymorphonuclear leukocyte (PMN)-mediated human pulmonary microvascular endothelial cell (HMVEC) damage and determine the role of soluble CD40 ligand (sCD40L).
Study Design And Methods:
PMPs were isolated from apheresis PLT concentrates. We used a two-insult in vitro model of HMVEC damage to investigate the effects of PMP and sCD40L and role of apocynin, an inhibitor of PMN respiratory burst. Their priming activities were measured using hydrogen peroxide production. The expression of intercellular cell adhesion molecule-1 (ICAM-1) and integrin αM (CD11b) were also determined.
Results:
Lipopolysaccharide (LPS)-activated HMVEC damage and PMN respiratory burst depend on the presence of PMP and the concentration of sCD40L. PMP-induced PMN-mediated HMVEC damage was significantly reduced by apocynin-treated PMNs (p < 0.05). The surface expression of ICAM-1 on HMVEC was increased by LPS stimulation. The expression of CD11b on PMNs was increased by PMP priming. Blocking ICAM-1 with a monoclonal antibody (MoAb) CD54 significantly reduced HMVEC damage (p < 0.05). The treatment of endothelial cells but not PMN with a MoAb targeting CD40 failed to prevent the HMVEC damage caused by PMPs (p > 0.05).
Conclusion:
PMPs carry a concentrated CD40L signal, promote PMN-mediated HMVEC damage, and may affect the development of transfusion-related acute lung injury.
Insights
Platelet microparticles (PMPs) concentrate soluble CD40 ligand (sCD40L), exacerbating polymorphonuclear leukocyte (PMN)-mediated damage to human pulmonary microvascular endothelial cells (HMVECs) and potentially contributing to transfusion-related acute lung injury.
Area of Science:
- Transfusion Medicine
- Immunology
- Cell Biology
Background:
- Stored platelets accumulate microparticles and biologic response modifiers (BRMs).
- BRMs can induce inflammatory reactions in transfusion recipients.
- Mechanisms of BRM effects remain unclear.
Purpose of the Study:
- Investigate platelet microparticle (PMP) effects on polymorphonuclear leukocyte (PMN)-mediated human pulmonary microvascular endothelial cell (HMVEC) damage.
- Determine the role of soluble CD40 ligand (sCD40L) in this process.
Main Methods:
- Isolated PMPs from apheresis platelet concentrates.
- Utilized a two-insult in vitro model of HMVEC damage.
- Measured PMN priming activity, hydrogen peroxide production, and expression of ICAM-1 and CD11b.
Main Results:
- PMP and sCD40L concentration influenced HMVEC damage and PMN respiratory burst.
- Apocynin-treated PMNs significantly reduced PMP-induced HMVEC damage.
- PMP priming increased CD11b expression on PMNs, and ICAM-1 blockade reduced HMVEC damage.
Conclusions:
- PMPs concentrate CD40L, promoting PMN-mediated HMVEC damage.
- This mechanism may contribute to transfusion-related acute lung injury (TRALI).
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