Staphylococcus aureus delays wound repair by harnessing the agr quorum sensing system to target keratinocyte lipid metabolism [bulkRNA-seq]

NHEKs wounded by scratch and incubated with CM for 24 hours were evaluated by bulk RNAseq. Principal component analysis of these data revealed wounded NHEKs exposed to S. hominis products clustered close to control keratinocytes, suggesting these groups have similar transcriptomes, while the presence of S. aureus products caused variation shift in the transcriptome to result in a distinct cluster away from control. This was supported by a heatmap of differential gene expression of S. aureus and S. hominis CM treatment showing broad S. aureus-mediated suppression of genes induced by S. hominis. Conversely, upregulation of many genes by S. aureus were downregulated by S. hominis. Bulk RNA-sequencing was performed on normal human keratinocytes cultured with or without sterile conditioned media from commensal and pathogenic staphylococcus treatment [in vitro].