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Dendritic cells aggregate inflammation in experimental osteoarthritis through a toll-like receptor (TLR)-dependent machinery response to challenges.

Authors
  • Nie, Fengfeng1
  • Ding, Fei2
  • Chen, Bo1
  • Huang, Shouguo1
  • Liu, Qingbai3
  • Xu, Changming4
  • 1 Department of Orthopedics, Linyi Central Hospital, Linyi, Shandong, 276400, China. , (China)
  • 2 Department of Orthopedics, Sheyang County People's Hospital, Yancheng, Jiangsu, 224300, China. , (China)
  • 3 Department of Orthopedics, Lianshui County People's Hospital, The Affiliated Lianshui County People's Hospital of Kangda College of Nanjing Medical University, Huai'an, Jiangsu, 223400, China. Electronic address: [email protected] , (China)
  • 4 Department of Orthopedics, Lianshui County People's Hospital, The Affiliated Lianshui County People's Hospital of Kangda College of Nanjing Medical University, Huai'an, Jiangsu, 223400, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Life sciences
Publication Date
Oct 11, 2019
Volume
238
Pages
116920–116920
Identifiers
DOI: 10.1016/j.lfs.2019.116920
PMID: 31610189
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Dendritic cells (DCs) and Toll-like receptor (TLR) participate in mediating inflammation process. However, the functional role of TLR expressed on DCs in osteoarthritis (OA) development has not been defined yet. The purpose of this study was to investigate the role and mechanism of TLR and DCs in the progression of experimental osteoarthritis (OA). Experimental OA model was induced by iodoacetate injection. Expressions of toll-like receptors in DCs of OA mice were detected by qRT-PCR and flow cytometry. TLR agonists lipopolysaccharide (LPS) and R848 or TLR antagonist FP7 were used, and the levels of TLRs and inflammatory cytokines were examined by qRT-PCR and ELISA. The expression levels of TLR family members were increased in DCs derived from synovial fluid of OA mice compared with the sham mice. In vitro, OA mice-derived DCs had increased production of inflammatory cytokine after TLR agonists LPS and R848 challenge, while TLR challenges did not affect DCs maturation. Inhibition of TLR by TLR antagonist FP7 blocked TLR challenges-induced increased inflammation in DCs. In mice, administration of FP7 attenuated LPS-induced inflammatory response and OA condition. Increased TLR expression in OA-derived DCs contributes to the inflammation condition and potentially acts as a therapeutic target for osteoarthritis. Copyright © 2019 Elsevier Inc. All rights reserved.

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