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Zhonghua Kou Qiang Yi Xue Za Zhi. 2018 Nov 9;53(11):753-759. doi: 10.3760/cma.j.issn.1002-0098.2018.11.007.
2
MicroRNAs and immunity in periodontal health and disease.微小 RNA 与牙周健康和疾病中的免疫。
Int J Oral Sci. 2018 Aug 6;10(3):24. doi: 10.1038/s41368-018-0025-y.
3
Effects of Micro RNAs and their Targets in Periodontal Diseases.微小RNA及其靶标在牙周疾病中的作用
Infect Disord Drug Targets. 2018;18(3):183-191. doi: 10.2174/1871526518666180405155327.
4
miR-146a regulates inflammatory cytokine production in Porphyromonas gingivalis lipopolysaccharide-stimulated B cells by targeting IRAK1 but not TRAF6.miR-146a 通过靶向 IRAK1 而非 TRAF6 调节牙龈卟啉单胞菌脂多糖刺激的 B 细胞中炎症细胞因子的产生。
Biochim Biophys Acta Mol Basis Dis. 2018 Mar;1864(3):925-933. doi: 10.1016/j.bbadis.2017.12.035. Epub 2017 Dec 27.
5
Bone and the Immune System.骨骼与免疫系统
Toxicol Pathol. 2017 Oct;45(7):911-924. doi: 10.1177/0192623317735316. Epub 2017 Oct 18.
6
Role of toll-like receptor 2 in inflammation and alveolar bone loss in experimental peri-implantitis versus periodontitis.Toll 样受体 2 在实验性种植体周围炎与牙周炎中的炎症和牙槽骨丧失中的作用。
J Periodontal Res. 2018 Feb;53(1):98-106. doi: 10.1111/jre.12492. Epub 2017 Sep 5.
7
The emerging roles of B cells as partners and targets in periodontitis.B细胞在牙周炎中作为伙伴和靶标的新作用。
Autoimmunity. 2017 Feb;50(1):61-70. doi: 10.1080/08916934.2016.1261841. Epub 2016 Dec 26.
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Local Induction of B Cell Interleukin-10 Competency Alleviates Inflammation and Bone Loss in Ligature-Induced Experimental Periodontitis in Mice.局部诱导B细胞产生白细胞介素-10的能力可减轻小鼠结扎诱导的实验性牙周炎中的炎症和骨质流失。
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9
Biomarker levels in gingival crevicular fluid of subjects with different periodontal conditions: A cross-sectional study.不同牙周状况受试者龈沟液中的生物标志物水平:一项横断面研究。
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Salivary Concentrations of Interleukin (IL)-1β, IL-17A, and IL-23 Vary in Relation to Periodontal Status.白细胞介素(IL)-1β、IL-17A和IL-23的唾液浓度随牙周状况而变化。
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microRNA-146a 调节脂多糖刺激的淋巴细胞细胞因子的产生。

MicroRNA-146a regulates the production of cytokines in lymphocytes stimulated by lipopolysaccharide.

机构信息

Dept. of Periodontology, Hospital of Stomatology, Tianjin Medical University, Tianjin 300070, China.

Dept. of Periodontology, Stomatological Center, Peking University Shenzhen Hospital, Shenzhen 518036, China.

出版信息

Hua Xi Kou Qiang Yi Xue Za Zhi. 2021 Feb 1;39(1):26-31. doi: 10.7518/hxkq.2021.01.004.

DOI:10.7518/hxkq.2021.01.004
PMID:33723933
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7905400/
Abstract

OBJECTIVES

This study aimed to investigate the effects of microRNA-146a (miR-146a) on the production of cytokines in lymphocytes stimulated by lipopolysaccharide (LPS).

METHODS

Lymphocytes were harvested from mouse spleen and cultured . The cells were treated with LPS, miR-146a mimic, or miR-146a inhibitor. Scramble RNA served as the negative control of mimic and inhibitor. The production of inflammatory cytokines was detected by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay.

RESULTS

Compared with non-LPS-stimulated group, LPS could increase the levels of interleukin (IL)-1β, IL-6, receptor activator NF-κB ligand (RANKL), and IL-10 (<0.05) and decrease the mRNA level of osteoprotectin (OPG) (<0.05). However, it did not significantly change the secretion of OPG. Compared with the negative control group, miR-146a mimic upregulated the levels of IL-10 and OPG (<0.05), downregulated IL-1β, IL-6, and RANKL (<0.05). Meanwhile, miR-146a inhibitor had a reverse effect on these cytokines (<0.05) in LPS-treated-lymphocytes.

CONCLUSIONS

MiR-146a can provide a suitable microenvironment for bone formation by preventing the inflammatory effects of LPS through the inhibition of IL-1β, IL-6, and RNAKL, thereby enhancing IL-10 and OPG.

摘要

目的

本研究旨在探讨 microRNA-146a(miR-146a)对脂多糖(LPS)刺激的淋巴细胞细胞因子产生的影响。

方法

从小鼠脾脏中采集淋巴细胞并进行培养。用 LPS、miR-146a 模拟物或 miR-146a 抑制剂处理细胞。 scramble RNA 作为模拟物和抑制剂的阴性对照。通过实时定量聚合酶链反应和酶联免疫吸附试验检测炎症细胞因子的产生。

结果

与未刺激 LPS 的组相比,LPS 可增加白细胞介素(IL)-1β、IL-6、核因子-κB 受体激活物配体(RANKL)和 IL-10 的水平(<0.05),并降低骨保护素(OPG)的 mRNA 水平(<0.05)。然而,它并没有显著改变 OPG 的分泌。与阴性对照组相比,miR-146a 模拟物上调了 IL-10 和 OPG 的水平(<0.05),下调了 IL-1β、IL-6 和 RANKL 的水平(<0.05)。同时,miR-146a 抑制剂在 LPS 处理的淋巴细胞中对这些细胞因子产生了相反的影响(<0.05)。

结论

miR-146a 可以通过抑制 IL-1β、IL-6 和 RNAKL 来防止 LPS 的炎症作用,为骨形成提供合适的微环境,从而增强 IL-10 和 OPG。