Lin Yanjun, Su Jingjing, Tang Shupin, Jiang Jun, Wei Wenwei, Chen Jiang, Wu Dong
Fujian Key Laboratory of Oral Diseases, School and Hospital of Stomatology, Fujian Medical University, Fuzhou 350004, China.
Department of Otorhinolaryngology-Head and Neck Surgery, The First Affiliated Hospital, Fujian Medical University, Fuzhou 350004, China.
Curr Issues Mol Biol. 2025 Jul 7;47(7):523. doi: 10.3390/cimb47070523.
Compelling evidence has demonstrated a bidirectional relationship between Sjögren's syndrome (SS) and periodontitis (PD). Nevertheless, the underlying mechanisms driving their co-occurrence remain unclear, highlighting the need for finding the hub gene. This study sought to examine the common genes and any connections between SS and PD. Differently expressed genes (DEGs) were analyzed by means of gene set enrichment analysis (GSEA), weighted gene co-expression network analysis (WGCNA), and least absolute shrinkage and selection operator (LASSO) methods. The test and validation sets were used to depict the receiver operating characteristic (ROC) curves. The immune cell infiltration was performed via the cell-type identification by estimating relative subsets of RNA transcripts (CIBERSORT) methodology. The relationships between immune infiltrating cells and the common gene were examined. Ninety-five common genes with similar expression trends were obtained after DEGs analysis, which were enriched in cytokine-cytokine receptor interaction, chemokine signaling pathway, proteasome, intestinal immune network for IgA production, and cytosolic DNA sensing pathway. Thirty-nine common genes were obtained after WGCNA. Sixteen shared genes of DEGs analysis and WGCNA were incorporated into the LASSO model to obtain the unique shared gene, C-C motif chemokine receptor 1 (), which overexpressed and owned predictable ROC curves in test and validation sets. The examination of immune cell infiltration underscored its crucial roles in the disturbance of immune homeostasis and the emergence of pathogenic circumstances with the simultaneous occurrence of SS and PD. overexpresses and serves as a critical pathogenic hub linking SS and PD, which may play a role through immune cell infiltration.
有力证据表明干燥综合征（SS）与牙周炎（PD）之间存在双向关系。然而，驱动它们同时出现的潜在机制仍不清楚，这凸显了寻找核心基因的必要性。本研究旨在探讨SS和PD之间的共同基因及任何联系。通过基因集富集分析（GSEA）、加权基因共表达网络分析（WGCNA）和最小绝对收缩和选择算子（LASSO）方法分析差异表达基因（DEG）。测试集和验证集用于描绘受试者工作特征（ROC）曲线。通过RNA转录本相对亚群估计的细胞类型鉴定（CIBERSORT）方法进行免疫细胞浸润分析。研究了免疫浸润细胞与共同基因之间的关系。DEG分析后获得了95个表达趋势相似的共同基因，这些基因富集于细胞因子-细胞因子受体相互作用、趋化因子信号通路、蛋白酶体、IgA产生的肠道免疫网络和胞质DNA传感通路。WGCNA分析后获得了39个共同基因。将DEG分析和WGCNA的16个共享基因纳入LASSO模型，以获得唯一的共享基因C-C基序趋化因子受体1（），其在测试集和验证集中过表达且具有可预测的ROC曲线。免疫细胞浸润分析强调了其在免疫稳态紊乱以及SS和PD同时发生时致病情况出现中的关键作用。 过表达并作为连接SS和PD的关键致病核心，可能通过免疫细胞浸润发挥作用。
