Summary This review discusses the role of microparticles in inflammation, coagulation, vascular function, and most importantly, their physiological and pathological functions in sepsis. Microparticles are proinflammatory, procoagulant membrane vesicles released from various cell types. They are detectable in normal individuals and basal levels correlate with a balance between cell proliferation, stimulation, and destruction. Haemostatic imbalance leads to various pathological states of inflammation and thrombosis including cardiovascular disease and sepsis, where circulating microparticles display both an increase in number and phenotypic change. Microparticles, mainly of platelet origin enable both local and disseminated amplification of the haemostatic response to endothelial injury through exposure of phosphatidylserine, tissue factor, and coagulation factor binding sites. Surface expression of membrane antigens by microparticles facilitates cytoadhesion, chemotaxis, and cytokine secretion to drive a proinflammatory response. Microparticles behave as vectors in the transcellular exchange of biological information and are important regulators of endothelial function and angiogenesis. The extent to which circulating microparticles contribute to the pathogenesis of sepsis and disseminated intravascular coagulation is currently unknown. Microparticles may in fact be beneficial in early sepsis, given that activated protein C bound to endothelium-derived microparticles retains anticoagulant activity, and increased circulating microparticles are protective against vascular hyporeactivity. Elevated levels of microparticles in early sepsis may therefore compensate for the host's systemic inflammatory response. Importantly, in vivo, septic microparticles induce deleterious changes in the expression of enzyme systems related to inflammation and oxidative stress, thus they may represent important contributors to multi-organ failure in septic shock.
|Number of pages||11|
|Journal||British Journal of Anaesthesia|
|Publication status||Published - Oct 2012|
- Endothelial dysfunction