Table 4.
Transfectant | Recognition by Opa variants | ||
---|---|---|---|
OpaB | OpaC | OpaI | |
CD66b | − | − | − |
R29F | +/− | − | +/− |
N32S | + | − | + |
A41G | +/− | − | +/− |
R44Q | − | − | − |
N32S+R29F | ++ | + | ++ |
N32S+A41G | ++ | + | ++ |
N32S+R44Q | + | − | + |
RF29F+N32S+A41G | ++/fp | ++ | ++/fp |
CD66e/b | ++/fp | ++ | ++/fp |
CD66e | ++/fp | ++ | ++/fp |
Interaction with Opa variants was determined by evaluating the percentage of receptor-positive cells that had significant amounts of associated gonococci (>5 bacteria per cell). Presence of receptor and bacteria was determined by immunofluorescence microscopy. The first column indicates the mutations made in CD66b; CD66e/b and CD66e indicate that the entire CD66b N-domain was replaced with either the chimeric N-domain mentioned in Table or the entire native CD66e N-domain. The results were tabulated as follows: ++/fp, all receptor-positive cells were infected plus numerous footprints were present; ++, 60–90% of receptor-positive cells were infected; +, 30–60% of receptor-positive cells were infected; +/−, 10–30% of receptor-positive cells were infected; −, no infected cells present. Infection experiments with recombinant MS11 Opa variants (reference 5) resulted in identical recognition patterns as those shown here for wild-type MS11 Opa variants. Results represent the mean of two to four independent experiments.