Irritable bowel syndrome (IBS) is the number one cause of consultation with the gastroenterologist. IBS is characterized by abdominal pain associated with impaired digestive functions. At the present time, there is no diagnostic marker for this pathology which drastically reduces the quality of life of patients, the inclusion of patients in the different subgroups of IBS being made on the basis of clinical questionnaires and by exclusion of other pathologies. This classification is one of the causes of the failure of clinical trials in this very heterogeneous group of patients. The increase in knowledge regarding this pathology and the identification of new therapeutic pathways represents an important challenge to improve the clinical care of these patients. Recent studies have shown that a dysfunction in the communication between the intestinal microbiota and the host could lead to the development of IBS. Thus, a better understanding of host-microbiota relationships could allow us to identify new therapeutic strategies. Numerous reports have established a link between the pathogenicity of IBS and the dysbiosis of the intestinal microbiota, a condition which refers to the decrease / loss of microbial diversity and richness. Nevertheless, there is a difference in the bacterial composition reported by the different studies. Due to the absence of a clear profile of dysbiosis of the intestinal microbiota in IBS and a functional redundancy of bacteria within the microbiota, our main objective is to identify the bacterial compounds implicated in the regulation of pain associated with IBS. Unlike inflammatory bowel disease, no increase in bacterial translocation could be observed in IBS patients indicating that if the bacteria have an impact on visceral pain, this is done through the action of the secreted molecules and / or transformed by bacteria on intestinal homeostasis. As many lipids are able to cross the intestinal barrier, we have attempted to characterize bacterial lipid metabolites. In a previous study we demonstrated that lipopeptides synthesized by bacteria can regulate the activity of sensitive nerves. Recently, we have quantified in the microbiota long chain fatty acids (LCFA) capable of regulating the functions of intestinal epithelial cells. We notably characterized a AGLC hydroxylated on the third carbon, C18-3OH, capable of activating the nuclear receptor PPAR. The objective of our project is therefore to study the role of the AGLC produced by the microbiota in the pathogenicity of IBS and their mechanisms of action on the host. As a first objective, we will establish the link between dysbiosis of the intestinal microbiota and visceral pain by characterizing the implications of the PPAR nuclear receptors in a mouse model of IBS. Then, we will quantify the bacterial AGLC and the abundance of microbiota bacteria during the genesis of IBS in mice. The correlation between these two parameters (bacterial strain and lipid compounds) and the symptoms of mice should allow us to characterize the AGLC and the bacteria involved in the pathogenicity of IBS. In a final part of our project, we will determine the agonist properties of bacterial AGLC on PPAR. Then, in vivo, in mice, we will assess the therapeutic potential of AGLC and of the bacteria involved in their production. This project, based on the complementarity of the different partners, should allow a better characterization of the pathogenicity of IBS. Our consortium offers a unique opportunity to understand the mechanisms of action of these bacterial AGLCs on pain to open new therapeutic perspectives in IBS.