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J Endod ; 37(10): 1370-5, 2011 Oct.
Article in English | MEDLINE | ID: mdl-21924184

ABSTRACT

INTRODUCTION: The 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. METHODS: Samples 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. RESULTS: The 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. CONCLUSIONS: In 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.


Subject(s)
Interleukin-8/biosynthesis , Nod1 Signaling Adaptor Protein/biosynthesis , Pulpitis/immunology , Pulpitis/metabolism , Analysis of Variance , Cells, Cultured , Chemokine CCL2/biosynthesis , Chemokine CCL2/genetics , Dental Pulp/cytology , Dental Pulp/immunology , Dental Pulp/metabolism , Fibroblasts/immunology , Fibroblasts/metabolism , Gene Expression Regulation , Humans , Interleukin-8/genetics , JNK Mitogen-Activated Protein Kinases/metabolism , MAP Kinase Signaling System , Nod1 Signaling Adaptor Protein/agonists , Nod1 Signaling Adaptor Protein/genetics , Phosphorylation , Statistics, Nonparametric , Up-Regulation , p38 Mitogen-Activated Protein Kinases/metabolism
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