Abstract
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. pyloriΔggt strains, H. suisΔggt 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 materialThe online version of this article (doi:10.1186/s13567-015-0163-6) contains supplementary material, which is available to authorized users.
Highlights
Helicobacter (H.) pylori is a Gram-negative bacterium that colonizes the stomach of more than half of the world’s population
The risk of developing gastric mucosa-associated lymphoid tissue (MALT) lymphoma is higher during non-H. pylori helicobacters (NHPH) infection compared to infection with H. pylori [4,5,6,7,8,9]
Discussion in the present study, H. suis strain HS5cLPΔggt was shown to be able to colonize the stomach of mice at similar levels compared to WT H. suis, it induced significantly less overall inflammation in both corpus and antrum. This suggests that the H. suis GGT is involved in the induction and regulation of the inflammatory response, without being an essential factor for colonization
Summary
Helicobacter (H.) pylori is a Gram-negative bacterium that colonizes the stomach of more than half of the world’s population. Infection with this bacterium can cause gastritis, peptic ulcer disease, gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma [1,2,3]. Besides H. pylori, non-H. pylori helicobacters (NHPH) have been detected in the stomach of humans and these bacteria cause similar gastric diseases. H. suis is the most prevalent gastric NHPH in humans. Pigs are the natural host of this bacterium, with prevalences reaching 90% or more [10] and
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