Trauma-hemorrhagic shock induces a CD36-dependent RBC endothelial-adhesive phenotype.

Area of Science:

• Physiology
• Immunology
• Pathology

Background:

• Microvascular dysfunction is a critical factor in multiple organ dysfunction syndrome.
• The precise mechanisms initiating intravascular occlusion and ischemic injury remain unclear.
• Red blood cell (RBC) adhesion to the endothelium is a potential trigger for these processes.

Purpose of the Study:

• To investigate the hypothesis that trauma-hemorrhage induces RBC-endothelial cell adhesion.
• To identify the molecular mechanisms underlying RBC-endothelial cell interactions after trauma-hemorrhage.

Main Methods:

• Prospective in vivo and in vitro animal studies.
• Analysis of blood samples from severely injured trauma patients.
• Assay of RBC adhesion to endothelial cells and measurement of adhesion molecules (e.g., CD36).

Main Results:

• Trauma-hemorrhage shock significantly increased RBC adhesion to endothelium in both rats and humans.
• Increased surface RBC CD36 expression was identified as the critical factor for adhesion.
• RBC CD36 binding to endothelial receptors (αVβ3 and VCAM-1) mediated adhesion.
• Gut-derived factors in intestinal lymph were identified as triggers for these RBC changes.

Conclusions:

• Trauma-hemorrhage shock rapidly induces RBC adhesion to endothelial cells.
• Enhanced RBC CD36 expression defines the RBC-adhesive phenotype post-trauma.
• Gut-derived humoral factors are responsible for the observed RBC phenotypic and functional changes.
• These findings offer insights into microvascular dysfunction in trauma, sepsis, and other stress conditions.