Abstract
The third component of complement, C3, is of central importance as an opsonin in the nonimmune host. Although gestational deficiencies in C3 levels are well recognized in neonates, defects in complement-mediated functions have not in every case correlated with low levels of complement proteins. Because opsonic functions of C3 are mediated through a reactive thiolester bond, we hypothesized that a biochemical dysfunction at this active site could explain the newborn’s predisposition to infection, even with relatively normal C3 levels. We therefore examined the biochemical integrity of the C3 thiolester in an assay independent of all other complement proteins. As measured by ELISA, mean C3 levels from 44 neonates (24-43 wk) were significantly lower in infants