Role of complement in multiorgan failure

Abstract

Multiorgan failure (MOF) represents the leading cause of death in patients with sepsis and systemic inflammatory response syndrome (SIRS) following severe trauma. The underlying immune response is highly complex and involves activation of the complement system as a crucial entity of innate immunity. Uncontrolled activation of the complement system during sepsis and SIRS with in excessive generation of complement activation products contributes to an ensuing dysfunction of various organ systems. In the present review, mechanisms of the inflammatory response in the development of MOF in sepsis and SIRS with particular focus on the complement system are discussed.

Figure 1

Summarizing illustration on the effects of excessive complement activation on various organ systems and the development of organ failure. For details see text. MBL: mannose-binding lectin, CNS: central nervous system, BBB: blood brain barrier, PMN: polymorphonuclear neutrophils, ARDS: acute respiratory distress syndrome, ATIII: antithrombin III, RES: reticuloendothelial system, GFR: glomerular filtration rate, ATN: acute tubular necrosis, FX: coagulation factor X, FII: coagulation factor II, TF: tissue factor, DIC: disseminated intravascular coagulation.