BK virus infection activates the TNFα/TNF receptor system in Polyomavirus-associated nephropathy

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• 作者：Andrea Ribeiro ; Monika Merkle ; Nasim Motamedi…
• 关键词：BK virus infection ; Polyomavirus ; associated nephropathy ; TNFα ; Toll ; like receptors
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2016
• 出版时间：January 2016
• 年：2016
• 卷：411
• 期：1-2
• 页码：191-199
• 全文大小：714 KB
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• 作者单位：Andrea Ribeiro (1)
  Monika Merkle (1)
  Nasim Motamedi (2)
  Hans Nitschko (2)
  Simone Köppel (1)
  Markus Wörnle (1)
  
  1. Medizinische Klinik und Poliklinik IV, Innenstadt, Klinikum der Universität München, Ziemssenstrasse 1, 80336, Munich, Germany
  2. Max von Pettenkofer-Institut, Munich, Germany
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Biochemistry
  Medical Biochemistry
  Oncology
  Cardiology
  
• 出版者：Springer Netherlands
• ISSN：1573-4919

文摘

Polyomavirus-associated nephropathy due to BK virus infection (BKVAN) is recognized as an important cause of significant kidney transplant dysfunction often leading to renal graft loss. The activation of innate immune defense mechanisms during BKVAN is still poorly understood and an altered regulation of inflammatory mediators by resident kidney cells upon viral infection can be expected to contribute to the onset and progression of disease. TNFα interacting with its receptors, TNF receptor 1 (TNFR1) and TNF receptor 2 (TNFR2), is largely accepted to be involved in viral responses, exhibiting both proinflammatory and immunosuppressive effects. Our aim was to examine the expressions of TNFα and TNFR1 and 2 in human collecting duct epithelial cells (HCDC) after infection with BKV as well as to study the effect of TNFα and poly(I:C), a synthetic analog of viral RNA, on the expressions of TNF receptors and proinflammatory cytokines and chemokines in HCDC. Quantitative RT-PCR analyses showed a downregulation of TNFα and an upregulation of both TNFR1 and 2 upon exposure of HCDC to the BK virus. TNFα stimulation induced the expressions of IL-6, IL-8, RANTES, and TNFR2. Poly(I:C) upregulated the expressions of both TNFR1 and TNFR2, a response that could be effectively blocked by siRNA to TLR3 and RIG-I, two double-stranded (ds) RNA receptors of the innate immune system. Poly(I:C)-dependent expression of TNFR2 but not TNFR1 was enhanced by TNFα. Taken together, our results suggest an involvement of TNF/TNFR system in virus-associated nephropathy. Keywords BK virus infection Polyomavirus-associated nephropathy TNFα Toll-like receptors