Killing of Neisseria meningitidis by Human Neutrophils: Implications for Normal and Complement-Deficient Individuals

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Abstract
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 Band 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. ⩾100% survival, respectively, at 30 min). Group B meningococci were resistant to complementmediated SBA, whereas group Y were susceptible. Deposition of C3 on serogroups Band Y was similar (28.5 ± 2.9 vs. 23.5 ± 2.7 C3 fluorescence units; P >.05); however, susceptibility to complement-dependent phagocytosis and complement-mediated SBA of serogroups Band 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.