TABLE 1.
Strains used in this study and their LPS phenotypes, expression of functional BabA, and ability to bind to healthy gastric mucosa
Strain testeda | LPS phenotype | Leb bindingb | In situ adhesion to gastric epitheliumb (mean ± SEM)
|
Reference(s) | ||
---|---|---|---|---|---|---|
Surface mucus cells | Parietal cells | Deep glands | ||||
17875 | No Lex or Ley | 44 ± 2.06 | 647 ± 24 | 0 | 0 | 4, 6 |
17875 babA KO | No Lex or Ley | <1 ± 0.03 | 36 ± 5 | 0 | 0 | 4, 6 |
ATCC 43504 | Lex, Ley | 25 ± 1.98 | 545 ± 13 | 0 | 0 | 1, 3 |
ATCC 43504 variant 1b | Ley | 29.5 ± 0.97 | 596 ± 22 | 21 ± 4 | 0 | 1, 3 |
ATCC 43504 variant 1c | Lex, Ley | 32.8 ± 1.0 | 607 ± 9 | 0 | 28 ± 2 | 1, 3 |
ATCC 43504 variant D1.1 | No Lex or Ley | 29.8 ± 1.22 | 537 ± 11 | 25 ± 5 | 79 ± 7 | 1, 3 |
ATCC 43504 variant K4.1 | i-antigen, H type I | 24.8 ± 1.5 | 512 ± 7 | 35 ± 3 | 113 ± 9 | 1, 3 |
ATCC 43504 babA KO | Lex, Ley | <1 ± 0.08 | 298 ± 19 | 0 | 0 | This study |
K4.1 babA KO | i-antigen, H type I | <1 ± 0.06 | 259 ± 28 | 34 ± 4 | 108 ± 13 | This study |
4187 | Lex, Ley | 3.3 ± 0.25 | 391 ± 8 | 0 | 18 ± 2 | 3 |
4187 KO 379/651 | i-antigen, H type I | 1.3 ± 0.12 | 538 ± 14 | 0 | 84 ± 9 | 3 |
NCTC 11637 | Lex, Ley | <1 ± 0.03 | 0 | 0 | 0 | 5 |
NCTC 11637 galE mutant | No Lex or Ley | <1 ± 0.07 | 0 | 0 | 0 | 5 |
NCTC 11637 rfbM mutantc | No Lex or Ley | <1 ± 0.03 | 0 | 0 | 0 | 5 |
Compared to the NCTC 11637 parent, variant 1b phase varies in an as-yet-unidentified N-acetylglusosaminyltransferase, 1c varies in α3-fucosyltransferase HP0651, K4.1 varies in α3-fucosyltransferase HP0379, and D1.1 varies both in N-acetylglusosaminyltransferase and HP0379. In strain 4187 KO 379/651, both HP0379 and HP0379 are inactivated. The Lewis phenotypes of all strains were tested repeatedly and found to be stable.
Based on two to four independent experiments. Bacterial adherence was defined as the number of bacteria per gastric pit.
rfbM codes for GDP mannose pyrophosphorylase, an enzyme specific for LPS biosynthesis.