Interaction of Neisseria gonorrhoeae with classical complement components, C1-inhibitor, and a monoclonal antibody directed against the Neisserial H.8 antigen.

Neisseria gonorrhoeae host adaptation and pathogenesis

“…In both the cervical epithelium and human serum, the alternative and classical complement pathways respond to N. gonorrhoeae infection by initiating the complement cascade to opsonize invading bacteria 18,100-102 . Studies in vitro have shown that N. gonorrhoeae interacts with several complement components 103 . N. gonorrhoeae evades complement-mediated killing through two general mechanisms: binding to and inactivating complement cascade components and preventing membrane attack complex formation, and presenting as ‘self’ by expressing molecules found in the host on the bacterial surface, and binding to complement regulatory proteins.…”

Human mannose-binding protein activates the alternative complement pathway and enhances serum bactericidal activity on a mannose-rich isolate of Salmonella.

“…Bactericidal activity in the presence of MBP is not simply a consequence of enhanced complement deposition (Joiner, K. A., and J. E. Schweinle, unpublished observations). In this respect, MBP functions analogously to bactericidal IgG for E. coli (44,45) and Neisseria gonorrheae (39,46). In contrast to the results with bactericidal IgG and E. coli (47), however, covalent complexes between C3 and MBP are not apparently responsible for the enhanced bactericidal activity.…”

Antibodies recognizing a variety of different structural motifs on meningococcal Lip antigen fail to demonstrate bactericidal activity

“…It is generally accepted that since the presence of serum bactericidal activity correlates with immunity to meningococcal disease (Goldschneider et al, 1969) the most desirable attribute of potential vaccine candidates is the ability to induce antibodies which promote complement-mediated bactericidal killing. In a study of gonococcal strains Schweinle et al (1989) reported that one anti-Lip mAb was bactericidal for two strains while Bhattacharjee et al (1990), using another mAb, found no killing of three different meningococcal strains tested. Given the highly conserved and repetitive structure of the Lip antigen it initially seemed likely that the mAbs used in such experiments might be directed against a single immunodominant epitope.…”

“…One report found passive protection against experimental meningococcal infection by the H.8 anti-lip mAb . More recent studies report that one anti-Lip mAb may promote complement-mediated killing of some gonococcal strains (Schweinle et al, 1989), while another is ineffective against meningococcal strains (Bhattacharjee et al, 1990).…”