Helicobacter pylori does not promote N-methyl-N-nitrosourea-induced gastric carcinogenesis in SPF C57BL/6 mice.

Helicobacter pylori (H. pylori) infection has been acknowledged as a promoter and an initiator for gastric carcinogenesis in experimental models using Mongolian gerbils with H. pylori strains TN2GF4 and ATCC 43504, which have + ve cagA and vacA phenotype s1 / m1. To get more insight into the role of H. pylori in gastric carcinogenesis, we studied the effect of H. pylori SS1, which has + ve cagA and vacA phenotype s2 / m2, on N-methyl-N-nitrosourea (MNU)-induced chemical gastric carcinogenesis using SPF C57BL / 6 mice. Thus, H. pylori SS1 was inoculated 1 week after the completion of MNU treatment to examine the promoting effect of this bacterium. The incidences of polypoid lesions, differentiated adenocarcinomas, and adenomatous hyperplasias were 67% (10 / 15), 47% (7 / 15) and 80% (12 / 15), respectively, in the MNU-alone group. The corresponding figures were 31% (8 / 26), 23% (6 / 26) and 35% (9 / 26) in the MNU + H. pylori group. The incidences of polypoid lesions and adenomatous hyperplasia were significantly different between the groups. Thus, the results indicate that H. pylori SS1 infection reduced susceptibility to chemical gastric carcinogenesis in this model. The discrepancy between the present result and previous results is likely to have been caused by differences in host factors and bacterial factors. Further study of the relationship between gastric carcinogenesis and H. pylori infection is needed.