BackgroundTo explore the role of leukemia inhibitory factor (LIF) in periodontitis via in vivo and in vitro experiments.MethodsThe 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.ResultsLIF 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.ConclusionsThese 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.

中文翻译：

---

白血病抑制因子通过巨噬细胞和牙周膜成纤维细胞的免疫调节来预防实验性牙周炎

背景通过体内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基因敲除小鼠及其野生型同窝小鼠的第二上磨牙结扎8 d。进行了微型计算机断层扫描（micro-CT）、组织学分析和定量实时聚合酶链反应（qRT-PCR）。在脂多糖（LPS）处理后，检测了小鼠骨髓来源的巨噬细胞和人牙周膜成纤维细胞（HPDLF）中促炎细胞因子的表达水平。结果LIF缺乏促进了结扎诱导的牙槽骨丢失、炎症细胞浸润、破骨细胞形成和胶原纤维降解。小鼠中，促炎细胞因子的表达较高，包括白介素-6 (IL6)、IL-1β (IL1B)、肿瘤坏死因子-α (TNFA)、基质金属蛋白酶 13 (MMP13) 和兰克/OPG比率。此外，当用 LPS 处理时，LIF 缺失导致来自股骨和牙槽骨的小鼠骨髓来源的巨噬细胞以及 HPDLF 中这些促炎细胞因子的表达水平更高。重组 LIF 减毒给药TNFA、IL1B， 和兰克/OPG结论这些研究结果表明，LIF缺陷通过调节巨噬细胞和牙周膜成纤维细胞的免疫炎症反应促进牙周炎的进展，LIF的应用可能成为牙周炎的辅助治疗以消除炎症。