J Dent Res:血清淀粉样蛋白A通过TLR2和TLR4促进慢性根尖周炎的发生

2018-09-22 lishiting MedSci原创

在现代细菌感染理念中,一直认为来源于病原体的病原相关分子模式(PAMPs)和来源于损伤/坏死宿主细胞的损伤相关分子模式(DAMPs)是诱导固有免疫反应的主要因素。然而,DAMPs在根尖周炎及边缘牙周炎中的作用还未可知。血清淀粉样蛋白A (SAA)是一种DAMP,它涉及多种慢性炎症性疾病的发展,如风湿性关节炎。在这篇研究中,作者利用人的尖周手术样本以及SAA和Toll-like receptors

在现代细菌感染理念中,一直认为来源于病原体的病原相关分子模式(PAMPs)和来源于损伤/坏死宿主细胞的损伤相关分子模式(DAMPs)是诱导固有免疫反应的主要因素。然而,DAMPs在根尖周炎及边缘牙周炎中的作用还未可知。血清淀粉样蛋白A (SAA)是一种DAMP,它涉及多种慢性炎症性疾病的发展,如风湿性关节炎。在这篇研究中,作者利用人的尖周手术样本以及SAA和Toll-like receptors (TLR)缺陷小鼠检测了SAA是否涉及到尖周损伤的发病机制中。

结果显示,SAA1/2在mRNA和蛋白水平上均局部表达于人尖周损伤内。SAA蛋白表达水平与损伤处的炎症程度正相关。在小鼠尖周炎症进展过程中,SAA1.1/2.1在野生小鼠(WT)的局部及全身均表达上调。虽然SAA1.1/2.1双敲和SAA3敲除小鼠表现出根尖周病变程度的明显减少,但这些小鼠与WT相比出现明显增多的炎症细胞浸润。重组人SAA1 (rhSAA1)在体外以剂量依赖的方式直接诱导WT嗜中性粒细胞的趋药性。并且,施加rhSAA1刺激会显著延长WT嗜中性粒细胞的存活。此外,rhSAA1会激活NF-κB通路,并以剂量依赖的方式促进巨噬细胞内IL-1α的产生。然而,TLR2/TLR4双敲明显减弱SAA介导的促炎症反应。

总的来说,SAA-TLR轴通过诱导炎症细胞浸润和延长细胞存活对慢性尖周炎症的形成发挥着重要作用。而PAMPs和DAMPs在牙齿/口腔炎症中的相互作用还需要进一步的研究。

原始出处

Hirai K, Furusho H, et al. Serum Amyloid A Contributes to Chronic Apical Periodontitis via TLR2 and TLR4. J Dent Res. 2018 Sep 6:22034518796456. doi: 10.1177/0022034518796456.

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    2019-02-24 仁医06
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    2019-08-21 lilianxiang
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