- pylori can induce gastric MALT lymphoma because of constant stimulation of antigen presentation leading to B cell expansion. Our working hypothesis is that a Helicobacter/Escherichia coli-coinfection promotes gastric lymphomagenesis.
The gastric and intestinal microbiota will be explored. Bacteriological, histological, molecular and metagenomic analyzes will allow us to answer several questions:
-does E. coli infection favor Helicobacter-induced gastric lymphomagenesis?
-does E. coli infection influence the gastric inflammatory response?
-are the virulence factors of E. coli, in particular colibactin, involved in these processes?
Our experimental approaches by metagenomics will allow to identify the nature of taxa and or functions associated with these microbiota modifications.
In perspective, it will be of major interest to validate the taxonomic and functional modifications observed within the microbial community in murine model, in biopsies of patients suffering from gastric MALT lymphoma.
Collaborations: Pr MJ Blaser, Rutgers University, New Jersey; Pr R Bonnet, CHU Clermont Ferrand ; Pr A Amiot, Hôpital Henri Mondor, Créteil, and Hôpital Saint Antoine, Paris-APHP; Pr B Huard, TRAIG, TIMC-IMAG, UMR 5525, university Grenoble-Alpes, La Tronche, France.