High-salt diet (HSD) was identified as a risk factor for obesity, hypertension, cardiovascular disease and was associated with autoimmunity. High salt intake influences the activation of pro-inflammatory immune cells through direct effects on T helper 17 cells, regulatory T cells (Tregs) and on antigen-presenting cells such as macrophages. In this study, our aim was to investigate the effects of HSD on the development of experimental autoimmune uveitis (EAU) in mice.
Native EAU or EAU by adoptive transfer (AT) was induced in mice by immunization with IRBP, in a SPF environment. Different parameters were examined comparatively between healthy and diseased mice, subjected to HSD versus control diet. The clinical grade of established EAU was determined at day 21. The antigen-specific response was assessed during the induction phase of the disease (d12) and in EAU mice (d21) by testing the proliferation rate of T cells in response to IRBP, their cytokine production and the presence of FOXP3+Tregs. An analysis of the intestinal microbiota on cecal samples was performed on naïve and EAU mice.
We observed a significant attenuating effect of HSD on the severity of native EAU but no effect on EAU by AT. There were no significant differences between diets in terms of proliferation rate nor cytokine production, but a trend to a higher HSD-linked proportion of Tregs cells. HSD affected the gut microbiota composition in each cohort. However, HSD effects on the gut microbiota composition were not systematically consistent between the two disease models.
Our data show a differential effect of HSD on the severity of native EAU and EAU by AT. Gut microbiota composition and Tregs could potentially impact the EAU severity following exposure to HSD.