The change of lymphocyte subsets and inflammatory cytokine in BK viruria

BackgroundPolyomavirus BK (BKV) infection as a serious complication after kidney transplantation. The process of infections in kidney transplant recipients is viruria, viremia, and BKVAN. The difference between BK negative and BK viruria in kidney recipients has not been defined. Patients and MethodsWe compared post-transplant lymphocyte subsets blood cytokinesurine cytokines levels of 19 renal transplant outpatients with (BK-positive) or without BK viruria (BK-negative, n=20), and 20 healthy controls (HCs). Group of BK-positive divide into low-(n=4) and high-level (n=15) According to BK viral load (VL).Immune cells including T cells, B cells, and natural killer (NK) cellsinterleukin-2(IL-2),IL-5,IL-6, IL-1{beta}, IL-10, IL-8, IL-17A,IL-4,IL-12P70, interferon-(IFN-), IFN-{gamma},and tumor necrosis factor- (TNF-)were determined by flow cytometry. ResultsBK-positive patients showed higher urine IL-1{beta} (P=0.040), IL-10 (P= 0.010), IFN-{gamma} (P =0.002), and TNF- (P =0.027) than BK-negative patients. Compared with HCs, BK-negative patients had lower urine IL-1{beta} (P=0.04), IL-10 (P=0.01), TNF- (P =0.027) and IFN-{gamma} (P =0.004),suggesting that cytokine expression regulation BK-infection. ConclusionBK-positive renal transplant recipients, especially those with high VL, showed strong inflammatory cytokine responses with increases of urine IL-1{beta}, IL-10, IFN-{gamma}, and TNF-. Our data suggest that monocyte- and Th-2-induced cytokines are involved in the pathogenesis of BKV-associated nephropathy.