BACKGROUND: Oral tolerance is the biological process explaining the non-responsiveness of gut lymphoid tissue to intestinal content. Our study tested a new approach for the enhancement of oral tolerance to a multiple sclerosis-triggering auto-antigen-myelin basic protein, by its oral administration with the Staphylococcal enterotoxin A. METHODS: Immune tolerance thus stimulated was assessed in adult BALB/c mice, by measuring different cytokines from the supernatant of mesenteric lymph nodes cells (IFN-γ, IL-4, IL-10, IL-17, and TGF-β), and in a SJL/E mouse model of experimental autoimmune encephalomyelitis, by evaluating the development of regulatory T cells in mesenteric lymph nodes and the clinical outcome of the intervention. RESULTS: We obtained a significant rise in the levels of IL-10 and TGF-β compared with control and a significant decrease of IFN-γ, IL-4 (p < 0.05). Regulatory T cells were increased compared with control (p < 0.05). These results were attributable both to myelin basic protein and to Staphylococcal enterotoxin A. The clinical outcome of experimental autoimmune encephalomyelitis was influenced only by the administration of myelin basic protein. CONCLUSION: In our experiment, Staphylococcal enterotoxin A enhanced the immune tolerance to myelin basic protein in the gut mucosa, but had no impact on the clinical evolution of experimental autoimmune encephalomyelitis.
BACKGROUND: Oral tolerance is the biological process explaining the non-responsiveness of gut lymphoid tissue to intestinal content. Our study tested a new approach for the enhancement of oral tolerance to a multiple sclerosis-triggering auto-antigen-myelin basic protein, by its oral administration with the Staphylococcal enterotoxin A. METHODS: Immune tolerance thus stimulated was assessed in adult BALB/c mice, by measuring different cytokines from the supernatant of mesenteric lymph nodes cells (IFN-γ, IL-4, IL-10, IL-17, and TGF-β), and in a SJL/E mouse model of experimental autoimmune encephalomyelitis, by evaluating the development of regulatory T cells in mesenteric lymph nodes and the clinical outcome of the intervention. RESULTS: We obtained a significant rise in the levels of IL-10 and TGF-β compared with control and a significant decrease of IFN-γ, IL-4 (p < 0.05). Regulatory T cells were increased compared with control (p < 0.05). These results were attributable both to myelin basic protein and to Staphylococcal enterotoxin A. The clinical outcome of experimental autoimmune encephalomyelitis was influenced only by the administration of myelin basic protein. CONCLUSION: In our experiment, Staphylococcal enterotoxin A enhanced the immune tolerance to myelin basic protein in the gut mucosa, but had no impact on the clinical evolution of experimental autoimmune encephalomyelitis.