Abstract

Objective: To investigate the role and mechanism of IL-17 and CXCR4 in chronic graft nephropathy (CAN) in rat models. Methods: CAN rat models were established using Fisher 344 to Lewis rats. In the control group(n=10), Lewis rats were performed isotransplantation. CAN rat models were established in experimental group(n=10). All the rats were havested 6 weeks after transplantation. Kidneys were examined by pathology to evaluate the injury of the renal allograft. SDF-1/CXCR4, IL-17 and α-SMA expression level in serum and renal graft were detected by immunohistochemical staining and Enzyme-linked immunosorbent assays(ELISA). The percent and the absolute amount of CD4(+) cells、CXCR4(+) cells and IL-17(+) cells were detected by flow cytometry. Results: The graft of the experiment group showed obvious pathological features of CAN. The protein expression levels of SDF-1/CXCR4 and IL-17 in the experiment group are significantly higher than in the control group. We could also observe the number of Th17 cells has a significant increase in the experiment group[blood (0.19±0.05)% vs (0.12±0.03)%; kidney (0.52±0.21)% vs (0.17±0.12)%]. The IL-17 level also showed the same differences between the experiment[blood (243.12±17.63) pg/ml, kidney (521.54±21.76) pg/ml]and the control group[blood (35.78±7.3) pg/ml, kidney (77.34±11.1) pg/ml]. Conclusions: The Th17 cells increase in the CAN rats model, maybe the SDF-1/CXCR4 has a chemotaxis to collect Th17 cells to the injured kidney. And its expression of IL-17 may promote the renal cells to transform into fibroblasts.

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