Influence of a deficiency of the second component of complement on the bactericidal activity of neutrophils in vitro.
Serum from three patients with a complete, selective deficiency of the second component of complement (C2) did not promote optimal killing of Staphylococcus aureus, 502A by neutrophilic polymorphonuclear leukocytes (PMN) in vitro. The addition of C2 reagent or the presence of heat-stable opsonin in the C2-deficient serum corrected the defective killing of S. aureus that was observed with patient or control PMN. PMN from the patients or control subjects killed bacteria with equal efficiency under conditions of optimal opsonization (normal pooled serum). However, twice-washed control PMN were better than patient PMN in killing S. aureus under circumstances of suboptimal opsonization (C2-deficient serum, heated C2-deficient serum, heated normal pooled serum, or no replacement of serum). The latter finding was due to residual C2 on the surface of twice-washed control cells. As repeated washing of control PMN progressively removed cell-associated C2, the staphylocidal effectiveness of the control RMN decreased to the level of patient PMN. In contrast to the findings with S. aureus, triply-washed PMN from patients or controls killed normal numbers of Escherichia coli, ON2, in C2-deficient serum.
D000818:Animals; D001770:Blood Bactericidal Activity; D003175:Complement C2 / Q000172:deficiency*; D003165:Complement System Proteins / Q000172:deficiency*; D004926:Escherichia coli; D007962:Leukocytes / Q000503:physiopathology*; D009895:Opsonin Proteins / Q000032:analysis; D013211:Staphylococcus aureus
D003175:Complement C2; D009895:Opsonin Proteins; D003165:Complement System Proteins