Lipoteichoic acid modulates inflammatory response in macrophages after phagocytosis of titanium particles through Toll‐like receptor 2 cascade and inflammasomes
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- Yasushi Naganuma
- Department of Orthopaedic Surgery Yamagata University Faculty of Medicine Yamagata Japan
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- Yuya Takakubo
- Department of Orthopaedic Surgery Yamagata University Faculty of Medicine Yamagata Japan
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- Tomoyuki Hirayama
- Department of Orthopaedic Surgery Yamagata University Faculty of Medicine Yamagata Japan
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- Yasunobu Tamaki
- Department of Clinical Medicine Yamagata Saisei Hospital Yamagata Japan
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- Jukka Pajarinen
- Department of Orthopaedic Surgery Stanford University School of Medicine California 94063
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- Kan Sasaki
- Department of Orthopaedic Surgery Yamagata University Faculty of Medicine Yamagata Japan
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- Stuart B. Goodman
- Department of Orthopaedic Surgery Stanford University School of Medicine California 94063
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- Michiaki Takagi
- Department of Orthopaedic Surgery Yamagata University Faculty of Medicine Yamagata Japan
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<jats:title>Abstract</jats:title><jats:p>Toll‐like receptor 2 (TLR2) and nucleotide‐binding and oligomerization domain‐like receptors with a pyrin domain 3 (NLRP3) inflammasomes have been presumed to participate in the pathogenesis of aseptic implant loosening. The aim of this study is to analyze the cellular localization of TLR2 and NLRP3 inflammasomes in the periprosthetic tissue from aseptically loose hip implants as well as the expression of these molecules in macrophages stimulated<jats:italic>in vitro</jats:italic>with titanium particles (Ti) coated with lipoteichoic acid (LTA). Using immunohistochemistry, immunoreactivity of TLR2 and NLRP3 inflammasomes was found in macrophages within the foreign body granulomatosis. Using RAW264.7 cells, stimulation with Ti increased the messenger RNA (mRNA) levels of TLR2 and TNF‐α. Stimulation with LTA‐coated Ti enhanced mRNA levels of NLRP3 and IL‐1β, whereas reinforced secretion of IL‐1β was not detected in spite of marked release of TNF‐α. Finally, the same cells with silenced Irak2, an adaptor protein in the TLR2 cascade, suppressed this NLRP3 upregulation. This study suggests that TLR2 and NLRP3 inflammasomes are factors involved in cross‐talk mediating the foreign body type response to wear particles. In addition, discrepant behavior in the release between TNF‐α and IL‐1β release may explain the variable pathomechanisms of aseptic implant loosening without acute inflammatory reactions. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 104A: 435–444, 2016.</jats:p>
収録刊行物
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- Journal of Biomedical Materials Research Part A
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Journal of Biomedical Materials Research Part A 104 (2), 435-444, 2015-10-22
Wiley
