Integrin-α9 (ITGA9) and its corresponding ligands are involved in inflammatory and immune responses. The present study aimed to investigate whether ITGA9 participates in the development of chronic periodontitis (ChP) and to explore the underlying mechanisms. We collected gingival tissue and gingival crevicular fluid in vivo from patients to determine the levels of ITGA9 and its ligands. We cultured primary periodontal ligament cells (PDLCs) in vitro and applied small interfering RNA to knock down ITGA9 in order to analyze the changes of inflammatory cytokines and explore the related cellular signaling pathways. The expression level of ITGA9 was significantly higher in the gingiva of patients with ChP than that of healthy individuals. ITGA9 knockdown in the PDLCs inhibited the secretion of interleukin (IL)-1β, IL-6, and IL-8. Western blot analysis indicated that this change could be attributed to the regulation of the mitogen-activated protein kinase (MAPK) signaling pathway. ITGA9 plays a regulatory role in the homeostasis of ChP. The results of the present study provide potential insights into the treatment of periodontitis.

Graphical abstract

整合素-α9 (ITGA9) 及其相应的配体参与炎症和免疫反应。本研究旨在调查 ITGA9 是否参与慢性牙周炎 (ChP) 的发展并探索其潜在机制。我们从患者体内收集牙龈组织和牙龈沟液，以确定 ITGA9 及其配体的水平。我们在体外培养原代牙周膜细胞（PDLCs）并应用小干扰RNA敲低ITGA9，分析炎性细胞因子的变化，探索相关的细胞信号通路。ChP患者牙龈中ITGA9的表达水平显着高于健康个体。PDLC 中的 ITGA9 敲低抑制了白细胞介素 (IL)-1β、IL-6 和 IL-8 的分泌。Western印迹分析表明，这种变化可归因于丝裂原活化蛋白激酶（MAPK）信号通路的调节。ITGA9 在 ChP 的稳态中起调节作用。本研究的结果为牙周炎的治疗提供了潜在的见解。

图形概要