論文

査読有り 国際誌
2016年9月

Elevated CD14 (Cluster of Differentiation 14) and Toll-Like Receptor (TLR) 4 Signaling Deteriorate Periapical Inflammation in TLR2 Deficient Mice.

Anatomical record (Hoboken, N.J. : 2007)
  • Daniel Rider
  • ,
  • Hisako Furusho
  • ,
  • Shuang Xu
  • ,
  • Alexander J Trachtenberg
  • ,
  • Winston Patrick Kuo
  • ,
  • Kimito Hirai
  • ,
  • Mako Susa
  • ,
  • Laila Bahammam
  • ,
  • Philip Stashenko
  • ,
  • Akira Fujimura
  • ,
  • Hajime Sasaki

299
9
開始ページ
1281
終了ページ
92
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1002/ar.23383

Apical periodontitis (periapical lesions) is an infection-induced chronic inflammation in the jaw, ultimately resulting in the destruction of apical periodontal tissue. Toll-like receptors (TLRs) are prominent in the initial recognition of pathogens. Our previous study showed that TLR4 signaling is proinflammatory in periapical lesions induced by a polymicrobial endodontic infection. In contrast, the functional role of TLR2 in regulation of periapical tissue destruction is still not fully understood. Using TLR2 deficient (KO), TLR2/TLR4 double deficient (dKO), and wild-type (WT) mice, we demonstrate that TLR2 KO mice are highly responsive to polymicrobial infection-induced periapical lesion caused by over activation of TLR4 signal transduction pathway that resulted in elevation of NF-kB (nuclear factor kappa B) and proinflammatory cytokine production. The altered TLR4 signaling is caused by TLR2 deficiency-dependent elevation of CD14 (cluster of differentiation 14), which is a co-receptor of TLR4. Indeed, neutralization of CD14 strikingly suppresses TLR2 deficiency-dependent inflammation and tissue destruction in vitro and in vivo. Our findings suggest that a network of TLR2, TLR4, and CD14 is a key factor in regulation of polymicrobial dentoalveolar infection and subsequent tissue destruction. Anat Rec, 299:1281-1292, 2016. © 2016 Wiley Periodicals, Inc.

リンク情報
DOI
https://doi.org/10.1002/ar.23383
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/27314637
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4982827
ID情報
  • DOI : 10.1002/ar.23383
  • PubMed ID : 27314637
  • PubMed Central 記事ID : PMC4982827

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