Figure 3

Microparticles and inflammation in sepsis. During sepsis, microparticles (MPs) are shed from a variety of activated or apoptotic cells. MPs may be considered as both the cause and the consequence of inflammation through multiple amplification and regulatory loops affecting vascular cells and functions. Thus, MPs contribute to the spread of inflammatory and prothrombotic vascular status and they may affect the smooth muscle tissue through adhesion molecules, activation of NF-κB and the expression of inducible nitric oxide synthase and cyclooxygenase-2, with an increase in nitric oxide and vasodilator prostanoids, leading to arterial hyporeactivity. MPs form microaggregates with circulating neutrophil granulocytes and platelets and are involved in the modification of the oxidative status, markedly increasing oxidative activity. Subunits of NADPH oxidase have been identified in MPs associated with increased production of reactive oxygen species. AA, arachidonic acid; COX = cyclooxygenase; ICAM, intercellular cell adhesion molecule; iNOS, inducible NO-synthase; LPS, lipopolysaccharide; NO, nitric oxide; PAF, platelet activating factor; R, Rantes; ROS, reactive oxygen species; TF, tissue factor; VCAM, vascular cell adhesion molecule.