Efeitos inflamatórios de dieta rica em sal na mucosa intestinal

Abstract

Excess intake of sodium is often associated with high risk for cardiovascular disease. More recently, some studies on the effects of high salt diets have also demonstrated that they are able to activate Th17 cells and increase severity of autoimmune diseases. In the present study, we showed that consumption of high salt diet (HSD) by mice triggered a gut inflammatory reaction associated with IL-23 production, recruitment of neutrophils and increased frequency of the IL-17producing type 3 innate lymphoid cells in the colon. Moreover, gut inflammation was not observed in IL-17-/- mice but it was present, although at lower grade, in RAG-/- mice suggesting that the inflammatory effects of high salt diet was dependent on IL17 but only partially on Th17 cells. Expression of SGK1, a kinase involved in sodium homeostasis, was not increased upon HSD ingestion at any of the time points tested. Colitis induced by oral administration of either dextran sodium sulfate (DSS) or 2,4,6trinitrobenzenesulfonic acid (TNBS) was exacerbated by HSD consumption and this effect was associated with increased frequencies of RORgt+ CD4+ T cells and neutrophils in the colon. Therefore, our results suggest that consumption of high-salt diet per se was able to trigger a mild inflammation in the colon and also to exacerbate colitis in mice by a mechanism dependent on IL-17 production but only partially dependent on Th17 cells.