Up-regulation of nucleotide-binding oligomerization domain 1 in inflamed human dental pulp |
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Authors: | Lee Ya-Yun Chan Chi-Hang Hung Shan-Ling Chen Yi-Chen Lee Yuan-Ho Yang Shue-Fen |
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Institution: | ∗Institute of Oral Biology, National Yang-Ming University, Taipei, Taiwan;†School of Dentistry, National Yang-Ming University, Taipei, Taiwan;‡Department of Stomatology, Division of Endodontics, Taipei Veterans General Hospital, Taipei, Taiwan;§Department of Economics, Fo-Guang University, Yilan, Taiwan |
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Abstract: | IntroductionThe innate immune response is activated by recognition of microbial components through specific pattern recognition receptors including nucleotide-binding oligomerization domain (NOD)-like receptors. However, the regulation of NOD-1 in inflamed human dental pulp remains poorly understood. This study aimed to evaluate the expression of NOD-1 in healthy and inflamed human dental pulps. In addition, the secretion of chemokines induced by NOD-1 and the related signaling pathways were studied.MethodsSamples of human dental pulp tissues were obtained from freshly extracted wisdom teeth. The protein localization of NOD-1 in the pulp tissues was detected by immunohistochemistry. In addition, human dental pulp fibroblasts were stimulated with NOD-1 agonist γ-D-glutamylmeso-diaminopimelic acid. Production of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) was determined by an enzyme-linked immunosorbent assay. The involvement of mitogen-activated protein kinase (MAPK) signaling pathways was examined by Western blot analysis, and the association of MAPK signaling with chemokine production was determined.ResultsThe results demonstrated the expression of NOD-1 in normal dental pulp, and up-regulated NOD-1 expression was observed in inflamed dental pulp. On stimulation with NOD-1 agonist, production of IL-8 and MCP-1 was induced in a dose-dependent manner. Moreover, phosphorylation of p38 MAPK and Jun N-terminal kinase (JNK) was enhanced by stimulation of NOD-1. With the treatment of p38 MAPK and JNK inhibitors, the NOD-1–induced IL-8 production was suppressed.ConclusionsIn response to microbial invasion, the expression of NOD-1 can be regulated in a ligand-inducible manner. NOD-1 might participate in pulp inflammation through chemokine production via MAPK signaling pathways. |
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Keywords: | Caries dental pulp interleukin-8 monocyte chemoattractant protein-1 nucleotide-binding oligomerization domain 1 |
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