Samin Golchin - Student of Microbiology / Member of Iranian Society of Microbiology

Sepsis, which is a highly heterogeneous syndrome, can result in death as a consequence of a systemic inflammatory response syndrome. The activation and regulation of the immune system play a key role in the initiation, development and prognosis of sepsis.[1]The roles of inflammation and coagulation in the pathophysiology of sepsis are described. Sepsis results when an infectious insult triggers a localized inflammatory reaction that then spills over to cause systemic symptoms of fever or hypothermia, tachycardia, tachypnea, and either leukocytosis or leukopenia. These clinical symptoms are called the systemic inflammatory response syndrome. Severe sepsis is defined by dysfunction ofone of the major organ systems or unexplained metabolic acidosis. The inflammatory reaction is mediated by the release of cytokines, including tumor necrosis factor-alpha, interleukins, and prostaglandins, from neutrophils and macrophages. The cytokines activate the extrinsic coagulation cascade and inhibit fibrinolysis. Monocyte-macrophage cells and dendritic cells play a key role in the innate immune response. These cells have the ability to phagocytosis bacteria and interact with their products through an interaction with their pattern-recognition receptors.[13]These overlapping processes result in microvascular thrombosis; thrombosis is one potential factor producing organ dysfunction. Activation of the coagulation system leads to consumption of endogenous anticoagulants (e.g., protein C and Anti-thrombin); this may be an important factor in the development of microvascular coagulation. Anti-inflammatory mediators as well as inflammatory mediators have a role in sepsis, and anexcess of either can result in poor patient outcomes. Sepsis is a complex syndrome involving activation of a variety of systems.[2]

Sepsis, Human Immune System, Blood infection, Immune response, Neutrophils, Macrophage