Department of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Changle People's Hospital, Weifang, Shandong, 262400, People's Republic of China.
Inflammation. 2021 Aug;44(4):1302-1314. doi: 10.1007/s10753-021-01417-y. Epub 2021 Feb 10.
Periodontitis is a widespread human chronic inflammatory disease of the tooth-surrounding tissues, which induces the destruction of periodontium and pathologic loss of teeth among adults. It has been reported that interleukin (IL)-17 was significantly increased in periodontitis patients compared to controls, while galectin-1 (Gal-1) was lower. Interestingly, it is found that Gal-1 treatment reduced systemic IL-17 levels. Hence, the aim of the present study was to explore the effect of Gal-1 on periodontitis development and investigate its underlying mechanism. In this study, Gal-1 was poorly expressed in lipopolysaccharide (LPS)-induced human periodontal ligament stem cells (hPDLSCs), and Gal-1 overexpression attenuated the production of inflammatory cytokines induced by LPS. Moreover, Gal-1 overexpression alleviated LPS-induced cell autophagy and apoptosis and reduced the expressions of IL-17A and IL-17R. Interestingly, IL-17A reversed the effect of Gal-1 on cell autophagy, inflammation, and cell apoptosis induced by the LPS challenge. In conclusion, Gal-1 inhibited LPS-induced autophagy and apoptosis of hPDLSC via regulation of IL-17A expression. Therefore, Gal-1 may have promising potential in regenerating periodontium.
牙周炎是一种广泛存在于人类的、围绕牙齿组织的慢性炎症性疾病，它会导致牙周组织破坏和成年人牙齿病理性缺失。据报道，与对照组相比，牙周炎患者的白细胞介素（IL）-17 显著增加，而半乳糖凝集素-1（Gal-1）水平较低。有趣的是，研究发现 Gal-1 治疗可降低系统性 IL-17 水平。因此，本研究旨在探讨 Gal-1 对牙周炎发展的影响，并研究其潜在机制。在本研究中，Gal-1 在脂多糖（LPS）诱导的人牙周膜干细胞（hPDLSCs）中表达水平较低，Gal-1 过表达可减轻 LPS 诱导的炎症细胞因子的产生。此外，Gal-1 过表达可减轻 LPS 诱导的细胞自噬和凋亡，并降低 IL-17A 和 IL-17R 的表达。有趣的是，IL-17A 逆转了 Gal-1 对 LPS 刺激引起的细胞自噬、炎症和细胞凋亡的作用。总之，Gal-1 通过调节 IL-17A 的表达抑制 LPS 诱导的 hPDLSC 自噬和凋亡。因此，Gal-1 可能在牙周组织再生方面具有广阔的应用前景。
