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.