GM‐CSF as a potential candidate of a vaccine‐induced reduction ofHelicobacter pyloriinfection

Abstract

To the Editor, Vaillant et al. 1 concluded that GM-CSF decreases Helicobacter pylori (H. pylori) load in chronically infected mice, induces β-defensin3, which displays an H. pylori inhibitory effect, and appears to play a role, most probably produced by the pathogenic Th17 cells, in the vaccine-induced decrease of H. pylori infection. GM-CSF is produced by both Th1 and Th17 cells, 2 and although Th1 lymphocytes and their induced cytokines contribute to anti-bacterial reaction, they also sustain chronic inflammatory reactions in the site of infection. 3 Helicobacter pylori infection induces a Th1-dominant response and gastric mucosa inflammatory process depends mostly on Th1 cell responses; in H. pylori-induced chronic gastritis, the Th1 cells predominate and seem to be critical for the development of gastritis and its associated pathologies. For instance, a predominantly activated H. pylori-specific Th1 response results in peptic ulcer disease 3 ; Th1 cells infiltration could contribute to the gastric cancer development and metastasis 3 ; and H. pylori CagY protein produces Th1 and Th17 responses in H. pylori-infected patients involved in gastric MALT lymphoma pathophysiology, also mentioned by the authors. 1 Thus, Th1/Th17 cell responses, at least in certain-infected patients, could be related to the development of more severe H. pylori-related disorders owing to the induction of immunopathologic reactions. 3