The dark side of C5a in sepsis.
Sepsis is a major clinical problem for which therapeutic interventions have been largely unsuccessful, in spite of promising strategies that were successful in animals, especially rodents. There is new evidence that sepsis causes excessive activation of the complement system and that this induces paralysis of innate immune functions in phagocytic cells due to effects of the powerful complement-activation product, C5a. This review describes our present understanding of how and why sepsis is a life-threatening condition and how it might be more effectively treated.
Ward
Peter A
PA
Department of Pathology, University of Michigan Medical School, 1301 Catherine Road, Ann Arbor, Michigan 48109, USA. pward@umich.edu
D000818:Animals; D003167:Complement Activation / Q000502:physiology; D015936:Complement C5a / Q000737:chemistry / Q000378:metabolism*; D003165:Complement System Proteins / Q000172:deficiency; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D044087:Receptor, Anaphylatoxin C5a / Q000737:chemistry / Q000378:metabolism; D018805:Sepsis / Q000378:metabolism* / Q000628:therapy
D015850:Interleukin-6; D044087:Receptor, Anaphylatoxin C5a; D015936:Complement C5a; D003165:Complement System Proteins