Our team studies the molecular mechanisms underlying bacterial infections. We focus on one of the most important human pathogen, Helicobacter pylori. This bacterium colonizes almost half of the world’s population and can survive and thrive in the stomach. Its infection associates with the majority of gastric diseases, including ulcers and gastric cancers. Hence, the bacterium was defined as a class 1 carcinogen by the world health organization.
We study two biological steps required for the infection process: the secretion of bacterial toxins and 2) the multiplication of the bacteria. We use a large panel of Biochemistry and Biophysics techniques (in particular X-ray crystallography) to understand the molecular mechanisms involved at the atomic level.
1) On the one hand, we try to determine how some of H. pylori secreted toxins penetrate human cells and disturb the functions of gastric cells. We try to solve the three dimensions structures of these toxins and of their complexes with host-receptors.
2) On the other hand, H. pylori multiplies in the gastric mucosa and must copy its genomic DNA at each cell division. Our work here aims at deciphering the role of the interactions occurring between several proteins involved in the initiation step of DNA replication: DnaA (initiator), DnaB (helicase) and a recently discovered regulator HobA. Our long-term goal is to obtain a model of the assembly of these proteins at the replication fork and use it to define new therapeutic targets against H. pylori.

Key words: Helicobacter pylori, Stomach cancer, Virulence factors, DNA replication, Biochemistry, X-ray crystallography, Host-pathogen interactions