Various studies proposed excessive complement activation during sepsis in humans (59) . Because of its potent inflammatory profile, C5a appears to be the most detrimental molecule and has been described as "too much of a good thing" (54) . When activated, C5a may lead to immune paralysis, multiorgan dysfunction and thymocyte apoptosis (37, 40) as well as disturbance of the coagulation and fibrinolytic cascades (34) .