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J Dent Res:M2巨噬细胞的诱导预防小鼠牙周炎模型中的骨丧失

2019-03-24 不详 网络

牙周炎的特征在于牙齿牙周支持组织的进行性破坏,其主要由响应于持续性细菌损伤的慢性炎症引起。最近已经清楚,牙周炎的发病机理与促炎性M1(经典激活的)巨噬细胞与抗炎M2(或者激活)的高比例相关。为了降低炎症活性,我们使用控释微粒(MP)局部递送C-C基序趋化因子配体2(CCL2)。已知CCL2促进M0或M2表型巨噬细胞对发炎部位的趋化性并局部诱导M2表型极化。结果显示,CCL2增加了M2表型巨噬细胞的

牙周炎的特征在于牙齿牙周支持组织的进行性破坏,其主要由响应于持续性细菌损伤的慢性炎症引起。最近已经清楚,牙周炎的发病机理与促炎性M1(经典激活的)巨噬细胞与抗炎M2(或者激活)的高比例相关。为了降低炎症活性,我们使用控释微粒(MP)局部递送C-C基序趋化因子配体2(CCL2)。已知CCL2促进M0或M2表型巨噬细胞对发炎部位的趋化性并局部诱导M2表型极化。

结果显示,CCL2增加了M2表型巨噬细胞的数量,降低了TNF-α分泌,并增强了RAW264.7细胞对CCL2 MP的趋化性。此外,我们通过接种牙龈卟啉单胞菌和小鼠磨牙周围的结扎,在2个动物模型中诱导牙周病。微型计算机断层扫描分析显示,与两种模型中的空白MP组和未治疗牙周炎组相比,CCL2 MP治疗组中牙槽骨损失显著减少。免疫组织学分析显示,在牙龈卟啉单胞菌诱导的模型的CCL2MP组中M2表型子集明显增加并且M1表型子集减少。此外,在两种模型中,抗酒石酸酸性磷酸酶染色显示CCL2 MP组中牙槽骨区域中的破骨细胞数量显着减少。此外,定量聚合酶链反应结果显示结扎模型中CCL2 MP组IL-1RA(白细胞介素1受体拮抗剂)mRNA表达显著增加,RANKL(核因子κ-b配体受体激活因子)mRNA表达减少。

总之,用CCL2 MPs操纵内源性M2表型巨噬细胞降低M1表型:M2表型比率,并防止小鼠牙周炎模型中的牙槽骨损失。CCL2 MP的递送提供了治疗牙周病的新方法。

原始出处:

Zhuang Z, Yoshizawa-Smith S, et al., Induction of M2 Macrophages Prevents Bone Loss in Murine Periodontitis Models. J Dent Res. 2019 Feb;98(2):200-208. doi: 10.1177/0022034518805984. Epub 2018 Nov 4.

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    2020-01-03 mei543
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    2019-03-24 CHANGE

    梅斯里提供了很多疾病的模型计算公式,赞一个!

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