| Popis: |
Objective: The aim of this study is to investigate the correlation between periodontal disease and chronic obstructive pulmonary disease (COPD) from the perspective of gene regulation, as well as the inflammatory pathways involved. Methods: Forty C57BL/6 mice were randomly divided into four groups: control group, chronic periodontitis (CP) group, COPD group, and CP&COPD group. Lung tissue samples were selected for messenger ribonucleic acid (mRNA) sequencing analysis, and differential genes were screened out. Gene enrichment analysis was carried out, and then crosstalk gene enrichment analysis was conducted to explore the pathogenesis related to periodontal disease and COPD. Results: Results of enrichment analysis showed that the differentially expressed genes (DEGs) in the CP group were concentrated in response to bacterial origin molecules. The DEGs in the COPD group gene were enriched in positive regulation of B cell activation. The DEGs in the CP&COPD group were concentrated in neutrophil extravasation and neutrophil migration. The mice in the three experimental groups had 19 crosstalk genes, five of which were key genes. Conclusions: Lcn2, S100a8, S100a9, Irg1, Clec4d are potential crossover genes of periodontal disease and COPD. Lcn2, S100a8, S100a9 are correlated with neutrophils in both diseases. Irg1 and Clec4d may bind to receptors on the surface of lymphocytes to produce cytokines and activate inflammatory pathways, this requires further research. |
