Enhancement of the invasive ability of Neisseria gonorrhoeae by contact with HecIB, an adenocarcinoma endometrial cell line.

Since Neisseria gonorrhoeae is an obligate pathogen, there is no animal model for identification of virulence factors for this bacterium. An alternative model for assessment of gonococcal virulence is invasion of the adenocarcinoma endometrial cell line, HecIB. Preincubation of gonococci with glutaraldehyde-fixed HecIB cells eliminated the six- to eight-hour lag in entry of bacteria into a fresh HeIIB monolayer seen with unpreincubated gonococci or gonococci preincubated in tissue-culture medium alone. Gonococci tightly bound to fixed HecIB cells were more invasive than cells free in the tissue-culture medium, suggesting that actual contact with HecIB cells was required for the enhancement of invasive ability. Chloramphenicol addition during the preincubation prevented the enhanced invasion. Preincubated gonococci were not more adherent to HecIB cells, suggesting that a stage in invasion after binding of gonococci to HecIB cells was enhanced. The enhanced invasion occurred only when gonococci were preincubated with HecIB cells and not with HEp-2, HeLa, Chang or CHO cells. This eukaryotic cell specificity for induction of enhanced invasion may indicate a role for invasion in gonococcal infection of the endometrium.