Studies on interaction of bacteria, serum factors and polymorphonuclear leukocytes in mothers and newborns

The bactericidal capacity of newborn infants' whole blood for E. coli was deficient compared to the mothers, and attempts were made to identify cellular or humoral factors responsible for this deficiency. Separated polymorphonuclear leukocytes from newborn infants were found to be similar to polymorphs from mothers in capacity to engulf and kill E. coli and other bacteria so that cellular deficiency was not evident. Comparison of the serum opsonic capacity of newborn infants' and mothers' sera revealed deficient opsonic capacity for E. coli in newborn sera. The mean opsonic titer for E. coli was 46.7 in mothers and 4.3 in neonates. Serum opsonic titers for Staph. aureus and group B streptococcus were similar. The opsonic capacity for all bacterial species was decreased when the sera were heated or decomplemented with immune complexes indicating the phagocytosis amplifying role of complement. The newborn-maternal difference in opsonic capacity for E. coli was presumably a result of deficient 19S antibodies, the primary opsonic antibodies for this organism. Maternal 19S serum fractions alone, however, showed no opsonic capacity for E. coli. Addition of a complement source (newborn serum absorbed with E. coli) revealed the opsonic capacity of these 19S maternal serum fractions for E. coli. Antibodies in 19S serum fractions therefore are efficient opsonins for E. coli; however, complement is necessary to demonstrate their opsonic potential.