Outer membrane vesicles alter inflammation and coagulation mediators

Area of Science:

• Microbiology
• Immunology
• Hematology

Background:

• Outer membrane vesicles (OMVs) are implicated in initiating the inflammatory response during sepsis.
• The role of OMVs in sepsis-associated hypercoagulability remains unexplored.
• Sepsis is characterized by both inflammation and a hypercoagulable state.

Purpose of the Study:

• To investigate the capacity of OMVs to induce endothelial mediators of coagulation and inflammation.
• To determine if OMVs can directly induce platelet activation.

Main Methods:

• Human umbilical vein endothelial cells (HUVECs) were treated with OMVs.
• Expression of tissue factor (TF), thrombomodulin, P-selectin, and E-selectin on HUVECs was analyzed.
• Supernatants from OMV-treated HUVECs were used to assess monocyte-platelet aggregate (MPA) formation in whole blood.

Main Results:

• OMVs significantly increased TF, E-selectin, and P-selectin expression on HUVECs.
• Thrombomodulin expression on HUVECs was significantly decreased by OMVs.
• OMV-induced endothelial activation led to increased MPAs, indicating platelet activation.

Conclusions:

• OMVs play a complex role in endothelial activation, influencing both inflammation and coagulation.
• While lipopolysaccharide on OMVs affects inflammatory markers like E-selectin, its impact on coagulation mediators is minimal.
• Endothelial activation by OMVs promotes platelet aggregation, potentially contributing to sepsis-induced hypercoagulability.