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Helicobacter pylori chronically persists in 50% of the human population and causes serious gastric and duodenal pathologies in 15% of infected people. Research on the immune response to the infection has mainly focused on the induction of CD4+ T cell responses. Human studies emphasize the potential clinical relevance of CD8+ cytotoxic T lymphocytes, however this cell type has barely been reported in studies employing mouse or gerbil models. Traditionally characterized as an extracellular bacterium, H. pylori has been identified inside epithelial and immune cells. Similarly to other intracellular bacteria, H. pylori infection of macrophages can alter autophagy and phagosome processing. A novel animal model of H. pylori infection demonstrates for the first time the induction of cytotoxic CD8+ T cell responses in pigs and localization of intracellular H. pylori within lymphoid aggregates. Here, we discuss novel mechanisms of host-H. pylori interactions that could lead to the induction of cytotoxic responses.

Original publication

DOI

10.4161/gmic.28899

Type

Journal article

Journal

Gut Microbes

Publication Date

05/2014

Volume

5

Pages

357 - 362

Keywords

CD8 T cells, Helicobacter pylori, Tbet, autophagy, gastric epithelial cells, gastritis, immunohistochemistry, intracellular bacteria, macrophages, pig models, Animals, CD8-Positive T-Lymphocytes, Disease Models, Animal, Gerbillinae, Helicobacter Infections, Helicobacter pylori, Host-Pathogen Interactions, Humans, Mice, Swine, T-Lymphocytes, Cytotoxic