TABLE 4.
Adhesion of wild-type S. gordonii DL1 and isogenic mutants to sHA in the presence of excess competing S. sanguinis cells
| S. gordonii strain | % of S. gordonii cells bound relative to control (mean ± SD) witha:
|
|
|---|---|---|
| 10-fold excess SK36 cells | 50-fold excess SK36 cells | |
| Control (no competitor) | 100.0 | 100.0 |
| DL1 (Challis) | 111.1 ± 6.3 | 89.8 ± 4.8 |
| scaA mutant (OB470) | 118.8 ± 14.1 | 90.4 ± 12.0 |
| abpAB mutant | 105.9 ± 5.6 | 77.6 ± 11.2** |
| sspAB mutant (UB1360) | 117.6 ± 13.6 | 74.6 ± 9.0** |
| cshAB mutant (OB277) | 102.8 ± 8.7 | 88.3 ± 2.9 |
| sspAB cshAB mutant (OB390) | 121.9 ± 34.4 | 87.4 ± 1.7** |
| srtA mutant | 102.6 ± 11.5 | 30.5 ± 7.9** |
| srtA-complemented strain | 105.0 ± 6.6 | 79.0 ± 15.0 |
| hsa mutant | 58.9 ± 8.2** | 29.5 ± 5.5** |
| hsa-complemented strain | 93.4 ± 13.9 | 94.7 ± 9.8 |
a
Radioactively labeled S. gordonii cells were incubated with sHA in the presence of a 10- or 50-fold excess of unlabeled S. sanguinis cells. Numbers of attached S. gordonii cells were then determined as described in Materials and Methods. As a control, S. gordonii strains were incubated with sHA in the absence of any competing cells, and these adhesion levels were set to 100%.
**
, value is significantly lower (P < 0.01) than that for controls in absence of competition.