Project description:The files in this archive examine six species within the genus Helicobacter to assay their histidine-rich proteins. They correspond to the manuscript "Expansion of nickel binding- and histidine-rich proteins during gastric adaptation of Helicobacter species" by Frederic Fischer, Egor Vorontsov, Evelyne Turlin, Christian Malosse, Camille Garcia, David L. Tabb, Julia Chamot-Rooke, Riccardo Percudani, Daniel Vinella and Hilde De Reuse.
The sequence databases for the Helicobacter species are based on reference or complete UniProt proteomes in FASTA format, supplemented with reannotations of Hpn and Hpn2 protein products.
The full list of RAW files, including their attribution to individual species and the type of experiment they represent, can be found in RAWs-Readme. We have included QuaMeter IDFree metrics to include basic statistics such as length of LC gradient, the number of MS/MS scans, etc.
Project description:Helicobacter pylori (H. pylori) is a human pathogen that infects almost half of the world’s population. Infection with H. pylori is frequently associated with chronic gastritis and can even lead to gastric and duodenal ulcers and gastric cancer. Although the persistent colonization of H. pylori and the development of H. pylori-associated gastritis remain poorly understood, it is believed that, in gastric mucosa, the modulated gastric epithelial cells (GECs) by H. pylori are key contributors. We used microarrays to detail the global programme of gene expression in Helicobacter pylori infected-gastric epithelial cell line AGS cells and identified up-regulated genes induced by Helicobacter pylori infection.
Project description:We are now trying to elucidate the mechanism of Helicobacter-induced gastritis and gastric cancer. To identify genes involved in these Helicobacter-associated diseases, we infected Helicobacter felis to INS-GAS (insulin-gastrin transgenic) mice (C57BL/6 background) which shows accelerated development of gastritis and gastric cancer.
Project description:Intestinal innate lymphoid cells (ILCs) contribute to the protective immunity and homeostasis of the gut, and the microbiota are critically involved in shaping ILC function. However, the role of the gut microbiota in regulating ILC development and maintenance still remains elusive. Here, we identified opposing effects on ILCs by two Helicobacter species, Helicobacter apodemus and Helicobacter typhlonius, isolated from immunocompromised mice. We demonstrated that the introduction of both Helicobacter species activated ILCs and induced gut inflammation; however, these Helicobacter species negatively regulated RORγt+ Group 3 ILCs (ILC3s), especially T-bet+ ILC3s, and diminished their proliferative capacity. Thus, these findings underscore a previously unknown dichotomous regulation of ILC3s by Helicobacter species, and may serve as a model for further investigations to elucidate the host-microbe interactions that critically sustain the maintenance of intestinal ILC3s.
