Demonstration and replacement of a funcional defect of the fifth component of complement in newborn serum. A major tool in the therapy of complement in septicemia

Abstract

Top of pageAbstract Previous studies from this and other laboratories have shown a relative deficiency in the opsonic activity of neonatal serum. The nature of this deficiency has been incompletely understood. The studies now reported show that the impairment of opsonic activity in neonatal serum involves a functional deficiency of the fifth component of serum complement (C5). (1) Opsonic activity of neonatal sera towards baker's yeast phagocytosis (Miller, 1969) was restored to normal by the addition of sera from mice with normal amounts of C5 (B10D2 new line) but not by addition of sera from a co-isogenic strain lacking C5 (B10D2 old line); (2) Utilizing highly purified human C3 & C5, re-constitution of opsonic activity of neonatal sera occurred only when C5 was added; (3) 5-day-old stored, ACD bank plasma was markedly deficient in re-constituting opsonic activity of neonatal serum. Fresh (<24 hrs) ACD plasma, however, effected significant re-constitution. The deficiency of 5-day-old plasma in opsonic re-constitution of neonatal sera was completely corrected by the addition of C5 containing mouse serum, or by purified human C5, but not by C5 deficient mouse serum. These studies demonstrate that the opsonic deficiency of neonatal serum involves a functional deficiency of C5 and that restoration of opsonic activity can be brought about by infusion of fresh plasma, which contains functionally active C5. A rationale is, therefore, presented for the use of fresh plasma in therapy of neonatal septicemia.