Microbiote intestinal et régime alimentaire dans la polyarthrite rhumatoïde

Gut microbiota, selected and then associated with the host in the best partnership, is essential in the regulation of the main physiological functions: metabolism, response to infection, immunity. Indeed, imbalance in the gut microbiota (dysbiosis) can trigger several diseases. Because of the milliards of microorganisms that colonize the surface of the body, innate immune recognition need to be tightly controlled both to ensure a symbiotic relationship between host and microbiota and to allow a rapid immune response in case of penetration of microorganisms into non-colonize sites. Bacterial components as well as microbial metabolites from dietary components constantly regulate immunity activity. In addition, microbiota is essential for the development and maturation of innate immune cells, can induce tolerance through epigenetic modification of pattern-recognition receptors (PRRs) and vice versa is modulated by PRRs. T and B cells, IgA, microbiota coexist in the gut mucosa to maintain immune homeostasis and strengthen barrier functions. Microbiota composition which is impacted by diet can modulate naïve T CD4 cell polarization into pathogenic Th17 or regulatory T cells. The immunomodulatory role of microbiota has been demonstrated in many experimental animal models and dysbiosis has been reported in rheumatoid arthritis. This link between gut microbiota, diet and arthritis raises the question of the effect of diet in rheumatoid arthritis, either by modifying the composition of the microbiota, restoring a normal microbiota, or offering personalized nutrition. Although microbiota knowledge opens new pathophysiological and therapeutic perspectives, it remains to specify the significance of the dysbiosis observed and to establish the causal link.