Abstract
In sepsis, inflammation and thrombosis are both the cause and the result of interactions between circulating (for example, leukocytes and platelets), endothelial and smooth muscle cells. Microparticles are proinflammatory and procoagulant fragments originating from plasma membrane generated after cellular activation and released in body fluids. In the vessel, they constitute a pool of bioactive effectors pulled from diverse cellular origins and may act as intercellular messengers. Microparticles expose phosphatidylserine, a procoagulant phospholipid made accessible after membrane remodelling, and tissue factor, the initiator of blood coagulation at the endothelial and leukocyte surface. They constitute a secretion pathway for IL-1β and up-regulate the proinflammatory response of target cells. Microparticles circulate at low levels in healthy individuals, but undergo phenotypic and quantitative changes that could play a pathophysiological role in inflammatory diseases. Microparticles may participate in the pathogenesis of sepsis through multiple ways. They are able to regulate vascular tone and are potent vascular proinflammatory and procoagulant mediators. Microparticles' abilities are of increasing interest in deciphering the mechanisms underlying the multiple organ dysfunction of septic shock.
Highlights
In the 1960s and 70s Wolf [1] was the first to describe platelet derivatives of less than 0.1 μm as procoagulant vesicles
MPs often convey tissue factor (TF) that may contribute to the dissemination of coagulopathy in sepsis [5,6] and cytokines up-regulating deleterious inflammatory responses [7]
Endothelial microparticles and inflammatory status Circulating MPs of endothelial origin may vary with respect to quantity and phenotype according to the endothelial response and have been reported in inflammatory diseases and disorders [47]; the endothelial response to inflammation stimuli may be immediate, delayed or reflect a chronic endothelial activation
Summary
In the 1960s and 70s Wolf [1] was the first to describe platelet derivatives of less than 0.1 μm as procoagulant vesicles. Endothelial microparticles and inflammatory status Circulating MPs of endothelial origin may vary with respect to quantity and phenotype according to the endothelial response and have been reported in inflammatory diseases and disorders [47]; the endothelial response to inflammation stimuli may be immediate, delayed or reflect a chronic endothelial activation They were reported to participate in the regulation of arterial tone in several diseases in which oxidative stress is involved, such as human acute coronary syndromes [48] or preeclampsia [49] associated with altered NO bioavailability [50]. In humans, a single endotoxin administration provokes a significant increase in endothelial-cell- or monocyte-derived MPs displaying potentiated TF [60] This state is worsened by the exhaustion and/or faulty activation of the two other regulatory molecules, antithrombin and APC. Subunits of NADPH oxidase have been identified in endothelial- and plateletderived MPs associated with increased production of reactive oxygen species [18,61] (Figure 3)
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