Leukemia inhibitory factor protects against experimental periodontitis through immuno-modulations of both macrophages and periodontal ligament fibroblasts.

IF 4.2 2区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Journal of periodontology Pub Date : 2024-03-15 DOI:10.1002/JPER.23-0607
Yanjing Ou, Le Fan, Xiaoqi Wang, Haibin Xia, Mengwen Cheng, Jing Huang, Youde Liang, Yining Wang, Yi Zhou
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Abstract

Background: To explore the role of leukemia inhibitory factor (LIF) in periodontitis via in vivo and in vitro experiments.

Methods: The second upper molar of LIF knockout mice and their wild-type littermates were ligated for 8 days. Micro-computed tomography (micro-CT), histological analysis, and quantitative real-time polymerase chain reaction (qRT-PCR) were performed. The expression levels of proinflammatory cytokines were examined in mouse bone marrow derived macrophages and human periodontal ligament fibroblasts (HPDLFs) after lipopolysaccharide (LPS) treatment.

Results: LIF deficiency promoted alveolar bone loss, inflammatory cells infiltration, osteoclasts formation and collagen fiber degradation in ligature-induced mouse, along with higher expressions of proinflammatory cytokines, including interleukin-6 (IL6), IL-1β (IL1B), tumor necrosis factor-α (TNFA), matrix metalloproteinase 13 (MMP13), and RANKL/OPG ratio. Additionally, LIF deletion led to higher expression levels of these proinflammatory cytokines in mouse bone marrow-derived macrophages from both femur and alveolar bone and HPDLFs when treated with LPS. Administration of recombined LIF attenuated TNFA, IL1B, and RANKL/OPG ratio in HPDLFs.

Conclusions: These findings indicate that LIF deficiency promotes the progress of periodontitis via modulating immuno-inflammatory responses of macrophages and periodontal ligament fibroblasts, and the application of LIF may be an adjunctive treatment for periodontitis to resolute inflammation.

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白血病抑制因子通过对巨噬细胞和牙周韧带成纤维细胞进行免疫调节,防止实验性牙周炎的发生。
背景:通过体内和体外实验探讨白血病抑制因子(LIF)在牙周炎中的作用:通过体内和体外实验探讨白血病抑制因子(LIF)在牙周炎中的作用:方法:将 LIF 基因敲除小鼠和野生型小鼠的第二上臼齿结扎 8 天。方法:将 LIF 基因敲除小鼠和野生型小鼠的第二上臼齿结扎 8 天,进行显微计算机断层扫描(micro-CT)、组织学分析和实时定量聚合酶链反应(qRT-PCR)。在脂多糖(LPS)处理后,检测了小鼠骨髓巨噬细胞和人牙周韧带成纤维细胞(HPDLFs)中促炎细胞因子的表达水平:结果:在韧带诱导的小鼠中,LIF缺失会促进牙槽骨丧失、炎性细胞浸润、破骨细胞形成和胶原纤维降解,同时促炎细胞因子的表达量也会增加,包括白细胞介素-6(IL6)、IL-1β(IL1B)、肿瘤坏死因子-α(TNFA)、基质金属蛋白酶13(MMP13)和RANKL/OPG比率。此外,LIF缺失会导致来自股骨和肺泡骨的小鼠骨髓巨噬细胞以及HPDLFs在接受LPS处理时这些促炎细胞因子的表达水平升高。给予重组 LIF 可减轻 HPDLFs 中的 TNFA、IL1B 和 RANKL/OPG 比率:这些研究结果表明,LIF 的缺乏会通过调节巨噬细胞和牙周韧带成纤维细胞的免疫炎症反应来促进牙周炎的进展。
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来源期刊
Journal of periodontology
Journal of periodontology 医学-牙科与口腔外科
CiteScore
9.10
自引率
7.00%
发文量
290
审稿时长
3-8 weeks
期刊介绍: The Journal of Periodontology publishes articles relevant to the science and practice of periodontics and related areas.
期刊最新文献
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