Killing of Neisseria meningitidis by human neutrophils: implications for normal and complement-deficient individuals.
The contributions of complement-dependent phagocytosis and serum bactericidal activity (SBA) to the killing of 62 strains of meningococci were examined by using C8-depleted or pooled human serum (PHS). The complement-dependent nature of killing by neutrophils was confirmed by restoring survival to control values by using heated serum. Serogroups B and 29E, but not A, C, Y, and W135, were ingested and killed by neutrophils in C8-depleted PHS (PHS-C8Dep; 41.7% +/- 7.3% and 60.5% +/- 17.8% vs. greater than or equal to 100% survival, respectively, at 30 min). Group B meningococci were resistant to complement-mediated SBA, whereas group Y were susceptible. Deposition of C3 on serogroups B and Y was similar (28.5 +/- 2.9 vs. 23.5 +/- 2.7 C3 fluorescence units; P greater than .05); however, susceptibility to complement-dependent phagocytosis and complement-mediated SBA of serogroups B and Y did not correlate. We also examined meningococcal phagocytosis by using serum from a C8-deficient patient. In contrast to PHS-C8Dep, this serum supported rapid phagocytic killing of serogroups A, C, Y, and W135 meningococci. This finding suggests that vaccinating individuals deficient in late-complement components may shift the burden of host defense from SBA to phagocytosis.
D001770:Blood Bactericidal Activity; D003167:Complement Activation; D003176:Complement C3 / Q000378:metabolism; D003185:Complement C8 / Q000172:deficiency; D003165:Complement System Proteins / Q000276:immunology*; D006801:Humans; D008854:Microscopy, Electron; D009345:Neisseria meningitidis / Q000276:immunology* / Q000648:ultrastructure; D009504:Neutrophils / Q000276:immunology* / Q000382:microbiology / Q000648:ultrastructure; D010587:Phagocytosis
D003176:Complement C3; D003185:Complement C8; D003165:Complement System Proteins