title: Interplay of complement and cytokines in the pathogenesis of septic shock.
abstract: Sepsis is a clinical syndrome that is usually induced by bacterial infections. It is generally assumed that the syndrome results from an excessive triggering of endogenous inflammatory mediators by the invading microorganisms. These mediators include substances released by activated monocytes, macrophages, endothelial cells and neutrophils such as cytokines, reactive oxygen species and proteases, as well as activation products of coagulation, fibrinolysis, contact and complement systems. Recent studies have suggested that cytokines and complement activation products may have overlapping biological activities. In addition, multiple interactions in vitro as well as in vivo between cytokines and complement have been described. Here we will review some of these recent studies and will discuss their relevance for the pathogenesis of sepsis and septic shock.
authors: Central Laboratory, Netherlands Red Cross Blood Transfusion Service, Amsterdam, Netherlands.
authors: J P
authors: JP
authors: de Boer
authors: G J
authors: GJ
authors: Wolbink
authors: L G
authors: LG
authors: Thijs
authors: J W
authors: JW
authors: Baars
authors: J
authors: J
authors: Wagstaff
authors: C E
authors: CE
authors: Hack
mesh_terms: D000818:Animals; D003167:Complement Activation; D003165:Complement System Proteins / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism*; D010450:Endopeptidases / Q000378:metabolism; D004727:Endothelium / Q000166:cytology / Q000378:metabolism; D006801:Humans; D008264:Macrophages / Q000378:metabolism; D009000:Monocytes / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism; D012772:Shock, Septic / Q000209:etiology* / Q000276:immunology
chemical_list: D016207:Cytokines; D003165:Complement System Proteins; D010450:Endopeptidases