COMPLEMENT ACTIVATION IN NEWBORN-INFANTS WITH EARLY-ONSET INFECTION

The complement system is an important element in host defense. Quantit ative deficiencies of total hemolytic complement activity and decrease d C3 levels were reported in sera from normal neonates. However, littl e is known about complement activation products in the newborn. In a p rospective study, complement activation products were determined in 32 healthy term neonates, in 41 neonates with colonization of their moth ers, in 15 colonized neonates, and in 10 neonates with early onset inf ection. In all newborns, EDTA plasma was obtained within the first 6 h of life. The anaphylatoxin C3a-desArg was determined with a novel ELI SA using an MAb reacting with a neoepitope of C3a-desArg. C3bBbP (alte rnative pathway convertase) and C1rsC1-inactivator (activation product of classical pathway) were measured with double-sandwich ELISA. C3 wa s determined by radial immunodiffusion. Plasma concentrations of C3a-d esArg were similar in healthy term neonates and healthy adults, wherea s diminished C3 levels were observed in the newborn infants. There wer e no significant differences between healthy neonates, neonates with c olonized mothers, and colonized neonates. In neonates with infection, a significant elevation of C3a-desArg was found at the onset of the di sease, resulting from alternative pathway activation. In contrast, the C1rsC1-inactivator complex showed no significant differences among he althy, colonized, and infected neonates. The anaphylatoxin C3a mediate s inflammatory reactions such as vasodilatation and an increase in mic rovascular permeability and might therefore play an important role in severe neonatal infection.