Abstract
Our aim was to assess whether the
Helicobacter pylori population recovered from experimentally infected mice show heterogeneity in
cag genotypes. Wild-type FVB/N mice were challenged with strain Hp1 and sacrificed 8 weeks later. Direct PCR on gastric tissue was performed using primers for
glmM and
cagA, and for these two genes and for
cagE and
virB11 using DNA from the infecting and the emerging strains. The gastric tissues of two of five mice were PCR+ for
glmM but not
cagA. For the infecting strain, the PCRs for all four genes studied were strongly positive, but the sweeps from the emerging strains from both mice gave weaker signals for
cagA and
cagE. Examination of single colonies showed reduced or absent signals for
cagA and
cagE in relation to
glmM and
virB11. Serial dilution PCR of sweep isolates from the mice showed a 10- to 100-fold decrease in
cagA signal compared to the infecting strain. The decrease of
cagA and
cagE, but not
virB11, amplification and lack of
cagA hybridization in Southern blots indicates a selective loss of the right half of the
cag island during murine infection. This phenomenon is consistent with host-induced adaptive changes of
cag genotype in the population of colonizing
H. pylori cells.