TGF-β1 Inhibits TLR-mediated Odontoblast Responses to Oral Bacteria

TGF-β1 Inhibits TLR-mediated Odontoblast Responses to Oral Bacteria
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DOI:
10.1177/0022034509334846
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发表时间:
2009-04-01
影响因子:
7.6
通讯作者:
Dale, B. A.
Dale, B. A.
中科院分区:
医学1区
文献类型:
--
作者:
Horst, O. V.;Tompkins, K. A.;Dale, B. A.

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TGF-β 1在牙齿发育和组织修复中发挥多种功能,但其在牙齿微生物防御中的作用尚未完全了解。成牙本质细胞将其细胞突起延伸到牙本质中,是第一个识别来自龋坏牙本质中的TGF-β 1和细菌的信号的细胞。本研究旨在确定TGF-β 1在调节成牙本质细胞对口腔细菌反应中的作用。我们表明,这些反应取决于微生物识别受体TLR 2和TLR 4的细胞表面上的表达水平。牙龈卟啉单胞菌、中间普雷沃菌和具核梭杆菌激活了两种TLR,但TLR 4发挥了更大的作用。缺乏细胞表面TLR 2与对变形链球菌、粪肠球菌和干酪乳杆菌的不良反应有关。TGF-β 1抑制TLR 2和TLR 4的表达,减弱成牙本质细胞的反应。我们的研究结果表明,TLR介导的炎症和TGF-β 1抗炎活性之间的平衡在牙髓炎症中起着重要作用。
TGF-beta 1 exerts diverse functions in tooth development and tissue repair, but its role in microbial defenses of the tooth is not well-understood. Odontoblasts extending their cellular processes into the dentin are the first cells to recognize signals from TGF-beta 1 and bacteria in carious dentin. This study aimed to determine the role of TGF-beta 1 in modulating odontoblast responses to oral bacteria. We show that these responses depend upon the expression levels of microbial recognition receptors TLR2 and TLR4 on the cell surface. Porphyromonas gingivalis, Prevotella intermedia, and Fusobacterium nucleatum activated both TLRs, but TLR4 played a greater role. Lack of cell-surface TLR2 was associated with poor response to Streptococcus mutans, Enterococcus faecalis, and Lactobacillus casei. TGF-beta 1 inhibited TLR2 and TLR4 expression and attenuated odontoblast responses. Our findings suggest that the balance between TLR-mediated inflammation and TGF-beta 1 anti-inflammatory activity plays an important role in pulpal inflammation.