Our research focuses on the pathogenesis of the bacterium Helicobacter pylori by studying both its bacterial virulence factors and the relation between this pathogen and its infected host. H. pylori colonizes the stomach of about half of the human population worldwide. H. pylori is an extraordinarily successful pathogen adapted to colonization of a unique niche, the acidic stomach. Infection by H. pylori is chronic and can evolve from gastritis to severe pathologies such as peptic ulcers and gastric cancer accounting for about 700,000 deaths per year worldwide. Gastric cancer develops in 1-3% of the infected individuals and constitutes the third cause of cancer related death in the world. H. pylori is till now the only bacterium to be recognized by IARC as a type 1 carcinogenic agent.
In addition to this public health issue, H. pylori is of particular interest because it is the only microorganism to persistently colonize the human gastric mucosa, its unique niche, which makes it an excellent mode organism to address fundamental questions related to its adaptation to such a hostile acidic environment.
Our objectives are to understand the mechanisms by which H. pylori persists and multiplies in the stomach and how this infection results in gastric cancer.
Current work in the lab focuses on:
Project 1: identification and characterization of H. pylori factors and mechanisms that allow this bacterium to persistently colonize the acidic gastric environment and generate gastric lesions as well as study of their evolutionary history.
Project 2: post-transcriptional regulation of gene expression, with a focus on non-coding regulatory RNAs and the mode of action of an RNA-degradosome.
Project 3 by the team of E. Touati: study of the host response and genotoxicity associated with the infection by H. pylori, in relation with the development of gastric cancer.
Our approaches comprise genetics, genomics, phylogenomics, bacterial physiology, biochemistry of proteins and RNA, cell biology, animal models and imaging.