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. 1999 Feb;67(2):834–843. doi: 10.1128/iai.67.2.834-843.1999

FIG. 3.

FIG. 3

(A) PilC purified from E. coli blocks the binding of N. gonorrhoeae to epithelial cells. (a and b) Binding patterns of piliated wild-type N. gonorrhoeae N138 without preincubation (a) and after preincubation (b) with 600 ng of PilC2His6 protein purified from E. coli ml−1 (b). (c to f) Competition of binding of N. gonorrhoeae N138 to human epithelial cells by PilC purified from N. gonorrhoeae. Shown are infected Hec-1B cells without pretreatment (c) and after pretreatment with 600 ng of PilC2His6 protein ml−1 (d) and infected RT112 cells without pretreatment (e) and after pretreatment with 600 ng of PilC2His6 protein ml−1 (f). (B) Competition of binding of N. meningitidis to human epithelial cells by PilC purified from N. gonorrhoeae. Target cells were ME-180 (a and b), Hec-1B (c and d), and RT112 (e and f) without pretreatment (a, c, and e) and after pretreatment with 600 ng of PilC2His6 purified from gonococci ml−1 (b, d, and f). (C) Competition of N. gonorrhoeae N138 binding to primary cornea epithelial cells by purified PilC2His6 protein. Cornea cells were from human origin. Binding of N138 to target cells without pretreatment (a) and after pretreatment with 12 μg of PilC2His6 purified from gonococci ml−1 (b) is shown.