Vitronectin promotes immunothrombotic dysregulation in the venular microvasculature
Bernd Uhl1,2, Florian Haring1,2, Julia Slotta-Huspenina3
1Department of Otorhinolaryngology, University Hospital, Ludwig-Maximilians-Universität München (LMU), Munich, Germany.
Frontiers in Immunology
|February 27, 2023
Summary
Vitronectin (VN) forms a scaffold in inflamed microvessels, promoting platelet and immune cell interactions. Blocking the VN receptor glycoprotein (GP)IIb/IIIa prevents microvascular clot formation in severe inflammatory diseases.
Area of Science:
- Immunology
- Hematology
- Pathology
Background:
- Microvascular immunothrombotic dysregulation contributes to severe systemic inflammatory diseases.
- Mechanisms of immunothrombosis in inflamed microvessels are not fully understood.
Purpose of the Study:
- To investigate the role of vitronectin (VN) in microvascular immunothrombosis during systemic inflammation.
- To explore the potential of targeting the VN-glycoprotein (GP)IIb/IIIa axis for therapeutic intervention.
Main Methods:
- Investigated VN's role in supporting platelet-immune cell-endothelial interactions in inflamed microvessels.
- Utilized blockade of the VN receptor GP IIb/IIIa to assess its impact on microvascular clot formation.
- Examined VN enrichment in pulmonary microvasculature of patients with severe systemic inflammation (pancreatitis, COVID-19).
Main Results:
- Vitronectin (VN) forms an intravascular scaffold under systemic inflammatory conditions.
- VN scaffold supports interactions between aggregating platelets, immune cells, and venular endothelium.
- Blockade of VN receptor GP IIb/IIIa prevented microvascular clot formation.
- VN was significantly enriched in the pulmonary microvasculature of patients with severe pancreatitis and COVID-19.
Conclusions:
- The VN-GP IIb/IIIa axis is crucial for microvascular immunothrombosis in systemic inflammation.
- Targeting this axis offers a promising therapeutic strategy for severe inflammatory conditions.
- VN-GP IIb/IIIa blockade is a feasible approach to counteract microvascular immunothrombotic dysregulation.
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