培養歯髄細胞における Streptococcus mutans および炎症性サイトカインによる CCL20 の発現

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  • CCL20 Production is Induced in Human Dental Pulp upon Stimulation by Streptococcus Mutans and Proinflammatory Cytokines
  • バイヨウ シズイ サイボウ ニオケル Streptococcus mutans オヨビ エンショウセイ サイトカイン ニヨル CCL20 ノ ハツゲン

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Introduction: Pulpitis is characterized as a marked infiltration of inflammatory cells in response to an invasion of caries-related bacteria. It is well known that chemokines regulate the trafficking of lymphocytes, and CC chemokine ligand 20 (CCL20) has been recently shown to play a crucial role in the recruitment of memory T cells and immature dendritic cells into inflammatory lesions. We previously reported that CCL20 was mainly expressed in microvasucular endothelial cells and macrophages accumulated in inflamed pulp tissues and its specific receptor; CCR6, was expressed on infiltrated lymphocytes. However, the mechanism of CCL20 expression remains unclear. Methods and Results: In this study, we investigated the expression of CCL20 in monocytes/macrophages, endothelial cells and pulpal fibroblasts after stimulation with Streptococcus mutans, a representative of caries-related bacteria, or pro-inflammatory cytokines. CCL20 mRNA was detected in inflamed pulp, but not in clinically normal pulp by reverse transcription-polymerase chain reaction. S. mutans induced human monocytic cells (THP-1), macrophage-like THP-1 differentiated with phorbol myristate acetate, and human umbilical vein endothelial cells (HUVEC) to produce an increased level of CCL20 as demonstrated by enzyme-linked immunosorbent assay. Lipoteichoic acid from S. mutans also elicited CCL20 production by HUVEC. Moreover, CCL20 production from cultured pulpal fibroblasts was increased by the stimulation with inetrleukin-1β and tumor necrosis factor-α. Conclusion: Our results indicate that CCL20 expression is induced by stimulation with caries-related bacteria invaded deeply into dentinal tubules and pro-inflammatory cytokines in inflamed pulpal lesions and may be involved in the progression of pulpitis via accumulation of inflammatory cells.

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