Department of Dermatology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.
State Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Diseases & Shaanxi Clinical Research Center for Oral Diseases, Department of Orthodontics, School of Stomatology, The Fourth Military Medical University, Xi'an, 710032, China.
Hereditas. 2023 Feb 10;160(1):7. doi: 10.1186/s41065-023-00266-z.
Increasing evidence indicates that psoriasis (PSO) and periodontitis (PD) are likely to occur together, however, the underlying mechanism remains unclear.
The expression profiles of PSO (lesion vs non-lesion, GSE30999, GSE14905) and PD (affected vs unaffected gingival tissue, GSE16134, GSE10334) were downloaded from the GEO database. First, we investigated the common differentially expressed genes (DEGs) of PSO and PD. Then, GO and KEGG enrichment analysis, protein interaction network (PPI) construction, and hub gene identification analysis were carried out. Finally, GO and KEGG enrichment analysis, miRNA interaction analysis, and transcription factors (TFs) interaction analysis for hub genes were performed.
Eighteen DEGs were identified for further analysis, including 15 up-regulated genes and 3 down-regulated genes. 9 hub genes were then identified via Cytohubba, including IL1B, CXCL1, CXCL8, MMP12, CCL18, SELL, CXCL13, FCGR3B, and SELE. Their functions are mainly enriched in two aspects: neutrophil chemotaxis and migration, chemokine activation and interaction. The enriched signaling pathways includes three categories: host defense, inflammation-related signaling pathways, and disease-related pathways. 9 common miRNAs based on experimental evidence and 10 common TFs were further identified in both PSO and PD.
Our study revealed possible comorbidity mechanisms in PSO and PD from the perspective of bioinformatics tentatively. The data can present new insight for joint prevention and treatment of in PSO and PD, as well as provide data support for further prospective studies.
越来越多的证据表明，银屑病（PSO）和牙周炎（PD）可能同时发生，但潜在机制尚不清楚。
从 GEO 数据库中下载 PSO（病变与非病变，GSE30999，GSE14905）和 PD（受影响与未受影响的牙龈组织，GSE16134，GSE10334）的表达谱。首先，我们研究了 PSO 和 PD 的常见差异表达基因（DEGs）。然后，进行了 GO 和 KEGG 富集分析、蛋白质相互作用网络（PPI）构建和枢纽基因识别分析。最后，对枢纽基因进行了 GO 和 KEGG 富集分析、miRNA 相互作用分析和转录因子（TFs）相互作用分析。
鉴定出 18 个 DEGs 进行进一步分析，包括 15 个上调基因和 3 个下调基因。然后通过 Cytohubba 鉴定出 9 个枢纽基因，包括 IL1B、CXCL1、CXCL8、MMP12、CCL18、SELL、CXCL13、FCGR3B 和 SELE。它们的功能主要富集在两个方面：中性粒细胞趋化和迁移、趋化因子激活和相互作用。富集的信号通路包括三个类别：宿主防御、炎症相关信号通路和疾病相关途径。根据实验证据进一步鉴定出 9 个共同的 miRNA 和 10 个共同的 TF 在 PSO 和 PD 中。
本研究从生物信息学角度初步揭示了 PSO 和 PD 可能的共病机制。这些数据为 PSO 和 PD 的联合预防和治疗提供了新的见解，并为进一步的前瞻性研究提供了数据支持。
