Studies were continued on the bactericidal activity of monoclonal antibodies directed against the H.8 proteolipid antigen of Neisseria gonorrhoeae. We found that levels of monoclonal which were bacteridical did not increase complement activation, exactly as we had previously reported with antibodies of different specificity. A new series of experiments was initiated testing the opsonic activity of the anti-H.8 monoclonal for human neutrophils, in conjunction with defined human complement fragments as opsonins. We used purified classical complement components to deposit defined complement fragments on the gonococcal surface. Of interest, strain JS3 activated the classical pathway in the absence of antibody. Although activation was prevented by C1 inhibitor, addition of antibody was able to override the control of the inhibitor. Monoclonal anti-H.8 was maximally opsonic for JS3 in the presence of bound C3b, while C3b alone, anti-H.8 alone, or anti-H8 plus C4b were intermediate in effect. Therefore, levels of anti-H.8 which do not increase C3 deposition in serum are opsonic and bactericidal for strain JS3. These studies resolve disagreement in the literature about the complement pathway which is activated by Neisseria gonorrhoeae in serum, and rigorously address the antibody and complement requirements for opsonization of this important human pathogen.
