Helicobacter pylori - Associated gastritis in mice is host and strain specific

The vacA and cagA geno- and phenotypes of two mouse-adapted strains of Heli cobacter pylori, SSI and SPM326, were determined. The SS1 strain, which had the cagA(+) and vacA s2-m2 genotype, induced neither vacuole formation in HeLa cells nor interleukin-8 (IL-8) production in KATO III cells, In contra st, H. pylori SPM326, with the cagA(+) and vacA s1b-m1 genotype, induced va cuoles as well as IL-S production in vitro. Furthermore, a spontaneous muta nt of SPM326, which produced a vacuolating cytotoxin but was not able to in duce IL-8 production (SPM326/IL-8(-)), was detected. C57B1/6 and BALB/c mic e were infected with these three strains to investigate the colonization pa ttern and the effect on the immune response in vivo. The SS1 strain coloniz ed the stomachs of all mice in large numbers which remained constant over t ime. Colonization with the SPM326/IL-8(+) and SPM326/IL-8(-) strains was le sser, or even absent, and decreased over time. At 5 weeks postinoculation a ll three H. pylori strains induced a mild increase of neutrophil count in t he gastric corpus of C57B1/6 mice, which disappeared by 12 weeks. At both 5 and 12 weeks postinoculation C57B1/6 mice colonized with SPM326/IL-8(+) sh owed an increased expression of major histocompatibility complex (MHC) clas s II antigen in the cardia which was accompanied by an increased number of T cells. C57B1/6 mice that were infected with SS1 and SPM326/IL-8- did not show chronic inflammation. BALB/c mice colonized with SS1 and SPM326/IL-8(- ) also showed an increase in neutrophil count at 5 weeks, which normalized again by 12 weeks postinoculation. At this time point SS1-infected mice sho wed inflammation in the corpus and antrum, At these sites an increased expr ession of MHC class II antigens and an increased number of T cells were obs erved. Although small lymphoid follicles were already observed 5 weeks afte r inoculation with SS1, their incidence as well as their number was increas ed at 12 weeks. These results show that inflammation induced hy H. pylori d epends both on the bacterial strain and the host.