High salt aggravates renal inflammation via promoting pro-inflammatory macrophage in 5/6-nephrectomized rat.

The increasing incident of chronic kidney disease (CKD) in recent years might be related to a change in dietary habits, known as excessive salt intake. Given excessive salt promotes pathogenic T cells responses. Since the importance of macrophage in the development of CKD, we addressed the effect of high salt loading on in a rat CKD model. We observed that 5/6Nx rats receiving a high salt diet showed strongly enhanced macrophage infiltration and activation in the renal tissue accompanied by deteriorated renal inflammation. Then we used the microarray expression profiling to detect the effect of additional Nacl on peritoneal macrophage derived from 5/6Nx. The NaCl treatment of macrophage extracted from 5/6Nx rat elicited a strong pro-inflammatory phenotype characterized by enhanced proinflammatory cytokine production, increased expression of molecules mainly involved in immune response process. This NaCl-induced pro-inflammatory macrophage phenotype was accompanied by increased phosphorylation of STAT1. Taken together, our study demonstrated that high salt intake promotes immune activation of macrophages through the STAT1 independently and exacerbates the kidney accompanied by promotion of inflammation. Thus, changes in diet may provide a novel strategy for the prevention or amelioration of CKD.