Comment

This study uses Helicobacter felisinfection of C57BL/6 mice as a model ofHelicobacter pylori infection in humans. Infection with H felis produces gastritis and gastric atrophy with mucous hyperplasia, metaplasia, and parietal cell loss. However, in mice preinfected with a nematode parasiteHeligmosomoides polygyrus there was reduced parietal cell loss and less mucous cell hypertrophy and metaplasia. Measurement of gastric mucosal cytokines revealed that preinfection with H polygyrus reduced the number of transcripts for Th1 associated cytokines and chemokines but increased transcripts for Th2-type cytokines. The authors suggest that concurrent Th2 immune responses elicited by the nematode downregulate the tissue damaging Th1 response elicited by H felis. In addition, the authors speculate that different rates of helminthic infection in different parts of the world might explain why, despite equally poor socioeconomic conditions and high rates of infection withH pylori, there are major differences in the incidence of gastric cancer.

However, before gastroenterologists recommend sending all their patients on a tropical holiday and suggest they eat all the unwashed and uncooked vegetables they can find, a few words of caution are needed. While this is an intriguing study, it is fair to say that the authors highlighted the positive aspects of their results and did not dwell on the negative aspects. The mice were studied at two time points, eight and 16 weeks after H felisinfection. At eight weeks, although chronic submucosal …