Abstract
Background
Recent studies have shown a close association between periodontal disease and respiratory diseases. Gingival fibroma is a form of periodontal disease, and the H1N1 virus is a common pathogen causing respiratory diseases. The objective of this study is to investigate the regulatory mechanisms of autophagy in common differential genes between gingival fibroma and H1N1 virus infection using bioinformatics methods
Method
Data sets of gingival fibroma and H1N1 virus infection were downloaded from GEO (Gene Expression Omnibus), and the differential genes between the two were identified using R language. The intersection of the differential gene sets of the two diseases with the autophagy-related gene set downloaded from Gene Cards was obtained. GO analysis and KEGG pathway enrichment analysis were conducted on the differential genes of the two diseases using R language. Immune infiltration analysis was performed on the differential genes of the two diseases, and a heatmap of the correlation between the common differential genes of gingival fibroma, H1N1 virus infection, and autophagy and immune cells was drawn using R language
Results
Data from two GEO datasets were analyzed, and the data of gingival fibroma were screened out286 differential genes (199 down-regulated genes, 87 up-regulated genes)and H1N1 virus infection388 differential genes (38 up-regulated genes and 350 down-regulated genes)There are four common differential genes in gingival fibroma, H1N1 virus infection and cell autophagyBST2, SOD2, SLC7A11, and MXD1The enrichment analysis results show that,The differential genes of gingival fibroma are mainly enriched in tissue development (biological processes), extracellular regions (cellular composition), through the incorporation or reduction of molecular oxygen acting on paired donors (molecular functions), and are enriched in fluid shear stress and atherosclerosis signaling pathways. The differential genes infected by H1N1 virus are mainly enriched in interspecies interactions (biological processes), nuclear endoplasmic reticulum membranes (cellular composition), signal receptor binding (molecular functions), and are enriched in influenza A, EB virus infection and other signaling pathwaysThe results of immune infiltration analysis showed that,Gingival fibroma is significantly related to dendritic cells and other immune cells, and H1N1 virus infectioninitial CD4 + T cellsDendritic cells and neutrophils are significantly related.
Conclusion
The regulatory mechanism of cell autophagy in the common differential genes between gingival fibroma and H1N1 virus infection can be analyzed by bioinformatics methods