Phenotypic changes of Helicobacter pylori components during an experimental infection in mice.
The bacterial pathogen Helicobacter pylori is highly adapted to the human stomach and the clinical isolates show a high diversity which could be due to adaptative changes of the strains passing from one host to another. In order to study these variations, experimental infection of mice was developed and provided three out of the eleven tested strains able to infect C57BL/6 mice: the Sydney strain which is known to be well adapted to mice and two freshly isolated strains from infected patients. Mice were orally infected with one of these three strains (infecting strains) and were killed 45 days later. H. pylori strains were isolated from the stomachs of mice (emerging strains). The three infecting strains were compared to the three emerging strains for protein and lipopolysaccharide profiles, antigenic profiles revealed by Western blot with monospecific sera and genetic status by testing for the cagA gene and the vacA genotype. During the 45 days of infection, H. pylori underwent phenotypic variations which may be attributed to the adaptation from a human to a mouse environment or from an in vitro to a mouse environment. Those variations consisted of an over-expression at the cell surface of a 180-kDa protein and of a decreased expression of proteins of 260 and 120 kDa. Moreover, antigenic variations were shown for the two freshly isolated strains from human: the CagA and VacA antigens were in the saline extracts of the infecting strains only while the UreA, UreB, HspA and HspB were in the saline extracts of both the infecting and the emerging strains. These variations may contribute to the adaptation of the strains to the mouse environment.
Janvier
B
B
Laboratoire de Microbiologie A, CHU La Milétrie, Poitiers, France.
Grignon
B
B
Audibert
C
C
Pezennec
L
L
Fauchère
J L
JL
D000818:Animals; D000940:Antigenic Variation; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000032:analysis / Q000235:genetics; D015153:Blotting, Western; D004591:Electrophoresis, Polyacrylamide Gel; D005260:Female; D005838:Genotype; D016480:Helicobacter pylori / Q000737:chemistry* / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D008070:Lipopolysaccharides / Q000032:analysis; D051379:Mice; D008810:Mice, Inbred C57BL; D010641:Phenotype; D016133:Polymerase Chain Reaction; D013997:Time Factors; D014774:Virulence
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D008070:Lipopolysaccharides; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori