ATROPHIC GASTRIC CHANGES IN BOTH HELICOBACTER-FELIS AND HELICOBACTER-PYLORI INFECTED MICE ARE HOST-DEPENDENT AND SEPARATE FROM ANTRAL GASTRITIS

Background/Aims-The role of host factors has been neglected in studies of the pathogenesis of Helicobacter associated disease. The aim of th is study was to assess the response of different mouse strains to infe ction with a single strain of Helicobacter felis. Method-Six strains o f inbred mice were infected with the identical H felis culture and wer e killed at one month, two months, and six months after infection to a ssess histopathological changes. In addition, two strains of mice were infected with a mouse adapted strain of H pylori and examined at six months after infection. Results-In SJL, C3H/He, DBA/2, and C57BL/6 inf ected mice, severe to moderlate chronic active gastritis was observed only in the body of the stomach, which increased in severity over time with specialised cells in the body glands being replaced. As the seve rity of this damage in the body increased and atrophic changes were se en, the level of bacterial colonisation of the antrum decreased. In co ntrast, in BALB/c and CBA mice, there was only mild gastritis in the a ntrum, no remarkable changes were detected in their body mucosa, and n o atrophy was seen over time. In both these strains of mice, heavy bac terial colonisation was seen, which tended to increase over the period of the experiment. Of particular importance in this experiment was th at bacterial colonisation was mainly restricted to the antrum yet the atrophy, when present, was only observed in the body of the stomach. H pylori infected C3H/He mice showed moderate colonisation of the antru m, which persisted up to six months with little development of atrophy . In contrast, H pylori in C57BL/6 mice showed excellent colonisation of the antrum at two months but six months after infection there was m oderate to severe body atrophy, which was associated with a loss of ba cteria from the antrum. Conclusions-These findings challenge current c oncepts of the development of Helicobacter induced atrophy in that act ive chronic gastritis of antrum in that active chronic gastritis of an trum or the body mucosa, or both, is not a prerequisite. They also sug gest an auto-immune basis for the pathology although no autoantibody o r antibody to the H+/K+ ATPase was detected. Loss of infecting helicob acters from the stomach together with development of an atrophic gastr itis in the body of the stomach is similar to the pattern found in cer tain H pylori infected human subjects.