<b>Supporting data for "Effects of </b><b>Akkermansia muciniphila </b><b>on </b><b>Porphyromonas gingivalis</b><b>-Induced Periodontal Disease: Immune Modulation and Microbiota Remodeling"</b>

The Dataset include the Elisa, qPCR, and WesternBlot result for the following study. The experimental section investigates the effects of Am on host immune responses and microbial interactions using both in vitro and in vivo models. In vitro studies with human gingival epithelial cells and human gingival fibroblasts demonstrate that Am can restore immune responses suppressed by Pg, enhance the expression of pro-inflammatory cytokines (IL-6, IL-8, MCP-1), and promote the recruitment of immune cells. Additionally, Am significantly reduces the adhesion and invasion of Pg, enhancing the resistance of host cells to infection. In vivo studies using a murine model of periodontitis reveal that Am administration mitigates alveolar bone resorption and reduces bacterial load in the periodontal compartment. The study shows that Am enhances the phagocytic activity of THP-1 differentiated macrophages via the MyD88 pathway, disrupting the TLR2/C5aR interaction exploited by Pg and promoting bacterial clearance.本数据集包含下述研究的酶联免疫吸附试验（ELISA）、实时定量聚合酶链式反应（qPCR）以及蛋白质印迹法（WesternBlot）实验结果。本实验部分通过体外（in vitro）与体内（in vivo）两种模型，探究了Am对宿主免疫应答及微生物互作的影响。以人牙龈上皮细胞及人牙龈成纤维细胞开展的体外实验表明，Am可逆转Pg介导的免疫应答抑制，上调促炎细胞因子（IL-6、IL-8、MCP-1）的表达，并促进免疫细胞招募。此外，Am可显著降低Pg的黏附与侵袭能力，增强宿主细胞的抗感染能力。采用牙周炎小鼠模型开展的体内实验显示，给予Am可减轻牙槽骨吸收，并降低牙周微环境中的细菌载量。本研究还证实，Am可通过髓系分化初级应答基因88（MyD88）通路增强经THP-1细胞诱导分化的巨噬细胞的吞噬活性，破坏Pg所利用的Toll样受体2（TLR2）/补体5a受体（C5aR）相互作用，进而促进细菌清除。