Our team studies how bacteria subvert host responses to cause disease. Our long-term goal is to unravel the molecular and cellular basis of the infectious process to develop new approaches to prevent the dissemination and virulence of these bacteria.
Our favorite pathogens
Brucella abortus
Brucella causes one of the most prevalent zoonoses worldwide, still endemic in many developing countries. Brucellosis can have a severe economic impact, affecting a wide range of animals, including ruminants, swine, and dogs. The presence of brucellosis in marine and terrestrial wildlife is also of concern. Brucella can invade and extensively replicate inside host cells by injecting specific proteins that tightly control cellular functions. Despite extensive intracellular replication, Brucella species have developed exquisite mechanisms to induce or inhibit inflammation depending on the tissue context, modulate cell signaling, and interfere with host metabolism. These proteins are the focus of our research.
Acinetobacter baumannii
Infections with multi-drug resistant bacteria are a leading cause of morbidity and mortality worldwide. A. baumannii is rapidly becoming a global health threat. It has a remarkable ability to persist in the environment and to acquire multi-drug resistance and virulence traits, enhancing its ability to cause life-threatening infections, particularly in intensive care units. Recent work suggests animals may present an important reservoir for the bacteria, potentially increasing antibiotic resistance spread. Characterizing A. baumannii-host interplay, considering its human-animal-environment context, is a central topic of our lab’s research.
News flash
September 2024:
Fun road trip to the Midwest Microbial Pathogenesis Conference at Indiana University, Bloomington.
Charline and Lison presented posters on Acinetobacter baumannii and Brucella abortus, respectively, and Suzana gave a talk on a Pseudomonas TIR domain protein!
Recent publication: Louche et al 2023
Extensive collaborative work identifying two new Brucella effectors targeting the host nuclear functions. We have named them Nyx, in honor of the Greek goddess of the night, daughter of Chaos, to illustrate the scientific path to their discovery!
We highlight that NyxA and NyxB display a novel nucleomodulatory function that promotes perturbation of the subcellular localization of nucleolar proteins during bacterial infection.
Structural studies identified the key interacting domains mediating Nyx targeting of the host de-SUMOylase SENP3, needed for efficient intracellular multiplication of Brucella abortus.