N. gonorrhoeae differentially subvert the effectiveness of
complement (C) and alter the inflammatory responses elicited in human
infection. Disseminated (DGI) isolates typically resist killing by normal serum (are serum-resistant), inactivate more C3b (to
iC3b preferentially bound via
amide linkages), generate less C5a, and result in less
inflammation at local sites.
Pelvic inflammatory disease isolates are serum-sensitive, inactivate less C3b (while maintaining active C3b via stable
amide linkages), generate more C5a, and result in more
inflammation at local sites. Sialylation of SS gonococci, presumed to occur in vivo, converts them to serum-resistant, but it does not change the patterns of C3b inactivation and therefore may not affect local
inflammation.
IgG antibody directed against gonococcal reduction modifiable
protein (Rmp) blocks C-mediated killing of N. gonorrhoeae. Anti-Rmp
blocking antibodies may harbor specificity for OmpA sequences shared with other neisserial species or Enterobacteriaceae or may be directed against unique Rmp upstream
cysteine loop specific sequences, or both. Preexisting
antibodies directed against Rmp facilitate transmission of gonococcal
infection to exposed women; exclusion of highly immunogenic Rmp
antigens from
vaccine candidates may be important.