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Helicobacter  ( H. )  suis  can colonize the stomach of pigs as well as humans, causing chronic gastritis and other gastric pathological changes including gastric ulceration and mucosa-associated lymphoid tissue (MALT) lymphoma. Recently, a virulence factor of  H. suis , γ-glutamyl transpeptidase (GGT), has been demonstrated to play an important role in the induction of human gastric epithelial cell death and modulation of lymphocyte proliferation depending on glutamine and glutathione catabolism. In the present study, the relevance of GGT in the pathogenesis of  H. suis  infection was studied in mouse and Mongolian gerbil models. In addition, the relative importance of  H. suis  GGT was compared with that of the  H. pylori  GGT. A significant and different contribution of the GGT of  H. suis  and  H. pylori  was seen in terms of bacterial colonization, inflammation and the evoked immune response. In contrast to  H. pylori Δ ggt  strains,  H. suis Δ ggt  strains were capable of colonizing the stomach at levels comparable to WT strains, although they induced significantly less overall gastric inflammation in mice. This was characterized by lower numbers of T and B cells, and a lower level of epithelial cell proliferation. In general, compared to WT strain infection,  ggt  mutant strains of  H. suis  triggered lower levels of Th1 and Th17 signature cytokine expression. A pronounced upregulation of B-lymphocyte chemoattractant CXCL13 was observed, both in animals infected with WT and  ggt  mutant strains of  H. suis . Interestingly,  H. suis  GGT was shown to affect the glutamine metabolism of gastric epithelium through downregulation of the glutamine transporter ASCT2.   Electronic supplementary material  The online version of this article (doi:10.1186/s13567-015-0163-6) contains supplementary material, which is available to authorized users.

Role of γ-glutamyltranspeptidase in the pathogenesis of Helicobacter suis and Helicobacter pylori infections