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Enhancement of the invasive ability of Neisseria gonorrhoeae by contact with HeclB, an adeno‐carcinoma endometrial cell line
Author(s) -
Chen J. C.R.,
Bavoil P.,
Clark V. L.
Publication year - 1991
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.1991.tb00800.x
Subject(s) - neisseria gonorrhoeae , biology , microbiology and biotechnology , cell culture , virulence , hela , cell , neisseria , bacteria , gene , biochemistry , genetics
Summary 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, HeclB. Pre‐incubation of gonococci with glutaraldehyde‐fixed HeclB cells eliminated the six‐ to eight‐hour lag in entry of bacteria into a fresh HeIIB monolayer seen with unpreincubated gonococci or gonococci pre‐incubated 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 ceils 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.