ASHRAF KARİMİNİK, RAMİNYAGHOBİ, SHAHRİAR DABİRİ
Experimental and Clinical Transplantation - 2018;16(1):50-54
Objectives: It has been hypothesized that BK polyomavirus infection leads to nephropathy in kidney transplant patients via various plausible mechanisms, such as stimulation of chemokines. The CXCL11 gene may also play a role in BK polyomavirus-associated nephropathy. Our aim was to compare expression levels of CXCL11 in BK polyomavirus-infected versus noninfected kidney transplant patients with nephropathy and healthy controls. Materials and Methods: We performed a cross-sectional study of 58 kidney transplant patients with the risk of BK polyomavirus infection; these patients were subgrouped as BK polyomavirus-infected (23 patients) and noninfected (35 patients). We also enrolled 30 healthy patients as controls in this study. The BK polyomavirus genome load was evaluated using a quantitative real-time polymerase chain reaction protocol in kidney transplant patients. We analyzed CXCL11 gene expression and protein levels using in-house SYBR green real-time polymerase chain reaction and enzyme-linked immunosorbent assay protocols. Results: The expression level of the CXCL11 gene was increased 22.37 ± 23.1-fold in BK polyomavirus-infected kidney recipients and 12 ± 24-fold in noninfected patients versus that shown in controls. Conclusion: From these results, we concluded that BK polyomavirus infection can induce CXCL11 gene expression in kidney transplant patients compared with that shown in patients without BK infection and healthy patients. However, further studies are needed to determine the accurate counteraction between BK polyomavirus infection and CXCL11in kidney trans¬plant patients.
