Spatial transcriptomic profiling reveals the pathophysiology of early-stage hidradenitis suppurativa

We investigated the role of the epithelium of nodules in Hurley stage I hidradenitis suppurativa (HS) by using spatial transcriptomics to analyse the profiles of epithelial cells and dermal-infiltrating immune cells. Compared with epidermal cysts, genes related to bacterial response, inflammatory mediators and neutrophil degranulation pathways were upregulated in the epithelial cells of early-stage HS nodules. Our analysis of dermal-infiltrating immune cells surrounding the epithelium of nodules revealed significantly elevated levels of B-cell-related genes. Similarly to the sinus tract formation observed in moderate-to-severe HS, we propose that the production of inflammatory mediators in early-stage HS may involve the activation of keratinocytes and their interaction with dermal-infiltrating immune cells.

Automated summary

We examined the role of epithelium in early-stage HS by analyzing the profiles of epithelial cells and dermal-infiltrating immune cells. Compared to epidermal cysts, early-stage HS nodules showed upregulation of genes related to bacterial response, inflammatory mediators, and neutrophil degranulation pathways in epithelial cells. Analysis of dermal-infiltrating immune cells surrounding the nodules revealed elevated levels of B-cell-related genes. Our findings suggest that the production of inflammatory mediators in early-stage HS involves the activation of keratinocytes and their interaction with dermal-infiltrating immune cells, similar to sinus tract formation observed in moderate-to-severe HS.