Transcriptome profiling of oral keratinocytes cocultured with Th17 cells during Escherichia coli infection
Oral lichen planus (OLP) lesions show chronic T cell–mediated inflammation and increased colonization by Escherichia coli, yet the mechanisms that enhance intracellular bacterial survival in oral keratinocytes remain poorly understood. In this study, we performed bulk RNA sequencing of the mouse oral keratinocyte line IMOK to examine how Th17 cells influence epithelial transcriptional responses during E. coli infection. IMOK cells were infected with an OLP-isolated E. coli strain and either cocultured with Th17 cells using a Transwell system (preventing direct cell–cell contact) or maintained without T cells, and total RNA was collected for transcriptome profiling. Gene expression patterns were compared between E. coli–infected IMOK cells with and without Th17 coculture to identify pathways affected by Th17-mediated modulation. Differential expression and functional analyses revealed Th17-associated signatures linked to changes in apoptosis, antimicrobial responses, and host defense pathways in oral keratinocytes. These data provide transcriptional insights into how Th17 cells influence epithelial responses to E. coli infection and may contribute to understanding immune–epithelial interactions relevant to OLP-associated inflammation. Overall design: IMOK oral keratinocytes were either maintained uninfected or infected with an OLP-isolated Escherichia coli strain. To investigate the influence of Th17-derived soluble factors on epithelial responses, infected IMOK cells were cocultured with Th17 cells using a Transwell system that prevented direct cell–cell contact. Total RNA was collected from E. coli–infected IMOK cells with Th17 coculture and from infected IMOK cells without T cells. Bulk RNA sequencing was performed to identify transcriptomic changes associated with Th17-mediated modulation of apoptosis, antimicrobial responses, and host defense pathways in oral keratinocytes.