The role of HS N-sulfation in the pathogenesis of RSV nephropathy

Abstract

Abstract Background Minimal change nephrotic syndrome (MCNS) is the most frequent cause of nephrotic syndrome in childhood. Previous studies have showed that respiratory syncytial virus (RSV) is the common trigger of MCNS. Methods Immunofluorescence of 3G10, 10E4 and HepSS1was performed in the kidneys, lungs and livers of RSV nephropathy rat model and the control. RSV fusion protein (RSVF) was detected by Western blot. The levels of HS domains in the kidneys and lungs of RSV nephropathy rat model were compared with that of RSVF. Results The expression of 10E4 and Hepss1 in kidney and lung of the normal rat was higher than 3G10. In the rat model of RSV nephropathy, RSVF of the kidneys and lungs showed stronger signal than the livers on day 8 and 14 after RSV infected. The expression of 3G10, 10E4 and Hepss1 in kidneys were obvious on day 4, then reduced from day 8 to 120. In the lungs the expression of 10E4 decreased continuously from day 8 to day 120, and Hepss1 reached the highest level on day 14 following by a reduction. While the level of RSVF was highest on day 8 when HS domains appeared weakly.Conclusions In the study, there were two main findings: (1) it was because of the Heterogeneity of HS, that is, rich N-sulfation in the kidney mediating RSV adhesion, which resulted in the progress of MCNS; (2) We firstly demonstrated that the damage directly of RSV and T-cell disorder in the pathogenesis of MCNS were equally important.