Molecular mechanisms in septic shock (Review)

Sepsis is a clinical syndrome defined by the presence of infection and systemic inflammatory response to infection and results from a complex interaction between the host and infectious agents. It is characterized by the activation of multiple inflammatory pathways, with an increased risk of mortality. The incidence of sepsis has been on an ever-increasing pathway in recent years. Sepsis can be induced by several clinical situations that predispose to its occurrence: malignant tumors, organ transplantation, AIDS, radiation therapy, burns, sores, polytrauma, diabetes mellitus, hepatic failure, renal failure, malnutrition, catheters or different invasive devices, and urinary catheters. The microorganisms involved in the pathogenesis of sepsis are Gram-positive cocci (Staphylococci, Streptococci) and Gram-negative bacilli (Klebsiella, Pseudomonas aeruginosa, E. coli), fungi (Candida), parasites, and viruses. Among mechanisms involved in septic shock production, two pathological phenomena appear: the profound decompensation of circulation and metabolic disturbances that evolve towards an irreversible state. The intimate mechanism of shock involves the activation of monocytes, macrophages and neutrophils by lipopolysaccharides of Gram-negative bacteria. The microvascular bed is directly involved in the etiopathogenesis of disorders of acute inflammatory states associated with or without sepsis. A better comprehension of sepsis pathophysiology, especially the molecular mechanisms of septic shock, allows for new therapeutic perspectives.