[:fr]Interface entre hôte et environnement dans les pathologie inflammatoires chroniques[:en]Host-Environment interface in chronic inflammatory disorders[:]
Team Viennois / Meinzer
Scientific areas :Manager(s)
Team composition
Emérite
Website
Des nombreuses preuves impliquent une perturbation de l’interaction immunitaire-microbienne de l’hôte et une dysbiose – terme désignant une altération du microbiote intestinal – dans la pathogenèse des MICI et d’autres troubles inflammatoires chroniques. Nos recherches se concentrent sur l’interface intestinale entre les compartiments externes et internes de l’intestin, et cherchent à expliquer comment cette interface influence la physiopathologie des maladies inflammatoires chroniques. Malgré notre intérêt pour les MICI, nous explorons également d’autres maladies inflammatoires chroniques liées à une altération du dialogue hôte-microbiote, comme l’arthrite. Ces deux conditions sont utilisées et considérées comme des maladies modèles de l’inflammation intestinale et extra-intestinale. Our main objective is therefore to understand how the intestinal interface can be a determining factor in the initiation and development of diseases associated with dysbiosis.
Dysbiosis early in life is now appreciated for its determining impact on gut health later in life. Several observations in humans and mice indicate that individuals with reduced contact with microbes in life develop a pathological imprint of IBD and other chronic disorders such as rheumatoid arthritis later in life. In contrast, greater bacterial diversity early in life prevents the development of disease in adulthood. Consequently, our project focuses on both early events and those occurring at the time of disease.
Our fundamental question, fuelled by clinical observations, is addressed along three axes:
1) Explore how the external world (environment, microbiota, diet) impacts the interface (OUTER). In an ongoing prospective exposure/non-exposure study, “MIKINAUTEs”, we seek to understand how exogenous factors (diet and exposome) may influence relapse and/or remission of IBD.
2) Understanding the interface itself (INTERFACE), with a particular focus on intestinal miRNAs and their role in host-microbiota interaction and, more generally, intestinal homeostasis.
3) To explore how deregulation of the interface impacts distant organs, leading to extra-intestinal pathologies (INNER) such as arthritis. This axis aims to determine how alterations in intestinal barrier function and bacterial translocation can promote IBD, and similarly arthritis and autoimmunity in genetically predisposed individuals.