Microparticles: markers and mediators of sepsis-induced microvascular dysfunction, immunosuppression, and AKI

Abstract

Sepsis is a severe and complex syndrome that lacks effective prevention or therapeutics. The effects of sepsis on the microvasculature have become an attractive area for possible new targets and therapeutics. Microparticles (MPs) are cell membrane-derived particles that can promote coagulation, inflammation, and angiogenesis; and can participate in cell-to-cell communication. MPs retain cell membrane and cytoplasmic constituents of their parental cells, including two pro-coagulants: phosphatidylserine and tissue factor. We highlight the role of microparticles released by endothelial and circulating cells after sepsis-induced microvascular injury, and discuss possible mechanisms by which microparticles can contribute to endothelial dysfunction, immunosuppression, and multi-organ dysfunction--including sepsis-AKI. Once viewed as cellular byproducts, microparticles are emerging as a new class of markers and mediators in the pathogenesis of sepsis.