DC‐SIGN reacts with TLR‐4 and regulates inflammatory cytokine expression via NF‐κB activation in renal tubular epithelial cells during acute renal injury. (5th October 2017)

• Record Type: Journal Article
• Authors: Feng, D.; Wang, Y.; Liu, Y.; Wu, L.; Li, X.; Chen, Y.; Chen, Y.; Chen, Y.; Xu, C.; Yang, K.; Zhou, T.
• Is Part Of: Clinical and experimental immunology. Volume 191:Number 1(2018:Jan.)
• Page Start: 107
• Page End: 115
• Publication Date: 2017-10-05
• Subjects: acute kidney injury -- DC‐SIGN -- NF‐κB -- renal tubular epithelial cells -- TLR‐4; Immunopathology -- Periodicals; 616.079
• DOI: 10.1111/cei.13048
• Languages: English
• ISSNs: 0009-9104

Abstract

Summary: In the pathological process of acute kidney injury (AKI), innate immune receptors are essential in inflammatory response modulation; however, the precise molecular mechanisms are still unclear. Our study sought to demonstrate the inflammatory response mechanisms in renal tubular epithelial cells via Toll‐like receptor‐4 (TLR‐4) and dendritic cell‐specific intercellular adhesion molecule 3‐grabbing non‐integrin 1 (DC‐SIGN) signalling. We found that DC‐SIGN exhibited strong expression in renal tubular epithelial cells of human acute renal injury tissues. DC‐SIGN protein expression was increased significantly when renal tubular epithelial cells were exposed to lipopolysaccharide (LPS) for a short period. Furthermore, DC‐SIGN was involved in the activation of p65 by TLR‐4, which excluded p38 and c‐Jun N‐terminal kinases (JNK). Interleukin (IL)‐6 and tumour necrosis factor (TNF)‐α expression was decreased after DC‐SIGN knock‐down, and LPS induced endogenous interactions and plasma membrane co‐expression between TLR‐4 and DC‐SIGN. These results show that DC‐SIGN and TLR‐4 interactions regulate inflammatory responses in renal tubular epithelial cells and participate in AKI pathogenesis. Abstract : DC‐SIGN and TLR4 interactions regulate the inflammatory response mediated by renal tubular epithelial cells and that this response participates in the AKI pathogenesis.