Knockdown of TNFR1 Suppresses Expression of TLR2 in the Cellular Response to Staphylococcus aureus Infection

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• 作者：Qianbo Chen ; Tianyong Hou ; Xuehui Wu ; Fei Luo ; Zhao Xie ; Jianzhong Xu
• 刊名：Inflammation
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：39
• 期：2
• 页码：798-806
• 全文大小：1,334 KB
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• 作者单位：Qianbo Chen (1) (2) (3) (4) (5)
  Tianyong Hou (1) (2) (3) (4)
  Xuehui Wu (1) (2) (3) (4)
  Fei Luo (1) (2) (3) (4)
  Zhao Xie (1) (2) (3) (4)
  Jianzhong Xu (1) (2) (3) (4)
  
  1. National and Local United Engineering Laboratory of Tissue Engineering, Department of Orthopaedics, Southwest Hospital, The Third Military Medical University, Chongqing, China
  2. Key Laboratory of Bone Tissue Engineering in PLA, The Third Military Medical University, Chongqing, China
  3. Laboratory of Tissue Engineering in Chongqing City, Chongqing, China
  4. Center of Regenetive and Reconstructive Engineering Technology in Chongqing City, Chongqing, China
  5. Department of Orthopedics, 155 Hospital of PLA, Kaifeng, China
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Rheumatology
  Internal Medicine
  Pharmacology and Toxicology
  Pathology
  
• 出版者：Springer Netherlands
• ISSN：1573-2576

文摘

Osteomyelitis is a common manifestation of invasive Staphylococcus aureus infection characterized by widespread bone loss and destruction. Phagocytes possess various receptors to detect pathogens, including the Toll-like receptors (TLRs). Previous studies have demonstrated that the S. aureus protein SpA binds directly to pre-osteoblastic cells via tumor necrosis factor receptor-1 (TNFR-1). In our present study, we investigated the relationship between TLR2 and TNFR-1 in S. aureus-infected osteoblasts. Our results showed that cell viability decreased, and apoptosis, expression of TLR2, and the secretion of inflammatory cytokines (TNF-α and IL-6) increased with increasing concentrations of S. aureus. The JNK pathway was also activated in response to S. aureus infection. Knockdown of TNFR1 not only inhibited the JNK pathway but also reduced TLR2 protein and RANKL levels in S. aureus-infected cells. Inhibition of the JNK pathway reduced the protein level of TLR2 and reduced TNF-α and IL-6 secretion in S. aureus-infected cells.