An Apparent Correlation Between Central Nervous System and Kidney's Erythropoietin and TNF Alpha Expression at Peak Experimental Autoimmune Encephalomyelitis Disease.

Experimental autoimmune encephalomyelitis (EAE) is an inflammatory demyelination disease associated with inflammatory reactions and attenuation of antioxidant capacity. Several lines of evidence show that organs such as the liver and kidneys can share their antioxidant activity to protect the central nervous system (CNS) against neurodegenerative diseases. The aim of this study was to examine the possible interplay of the kidneys and CNS in pathogenesis of EAE. For this purpose, EAE model was induced in C57BL/6 mice, and expression of erythropoietin (EPO), TNF-α, and NFκB-1 was determined in the kidney and CNS at early and peak stages of the disease. Besides, changes in serum level of EPO and total antioxidant capacity (TAC) were measured by different clinical scores. Real-time PCR (qPCR) results showed a substantial increase in TNF-α and NFκB-1 expression in mice at EAE peak stage compared to sham (control). There was a positive correlation between kidney-EPO and CNS-inflammatory factor expression in EAE-induced mice. In general, EPO expression was relatively higher in the kidneys compared to CNS tissue in sham group. There was a significant upregulation in expression of EPO in the brain, spinal cord, and kidneys particularly at peak stage. Accordingly, changes in serum TAC were consistent with serum EPO concentration. This data may suggest that there is an EPO-mediated cross-talk between the kidney and CNS during EAE pathogenesis.