Background
Pathogenesis and persistence of many skin diseases are related to Staphylococcus aureus (S. aureus) colonization. S. aureus infection can cause varying degrees of changes in cell gene expression, resulting in complex changes in cell phenotype and finally changes in cell life activities. Materials and
Conclusion
The identified genes and pathways are potential drug targets for treating skin inflammation caused by S. aureus and should be investigated further.
Methods
The transcriptomes of healthy and Staphylococcus aureus (S. aureus)-infected murine skin tissues were analyzed. We identified 638 differentially expressed genes (DEGs) in the infected tissues compared to the control samples, of which 324 were upregulated and 314 were downregulated, following the criteria of P < 0.01 and |log2FC| > 3. The DEGs were functionally annotated by Gene Ontology (GO), KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway and the protein-protein interaction (PPI) network analyses.
Results
The upregulated DEGs were mainly enriched in GO terms, such as response to stimulus, immune system process and signal transduction, as well as in the complement and coagulation cascade pathway. Thus, S. aureus infection likely activates these pathways to limit the influx of neutrophils and prevent skin damage. Four clusters were identified in the PPI network, and the major hubs were mainly related to cell cycle and proliferation, and mostly downregulated. The expression levels of Nox4, Mmrn1, Mcm5, Msx1 and Fgf5 mRNAs were validated by qRT-PCR and found to be consistent with the RNA-Seq data, confirming a strong correlation between the two approaches.