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Replication Stress in Hair-Follicle-Stem-Cell Leads to IFI16-STING dependent inflammation in Hidradenitis Suppurativa

ABSTRACT: Replication Stress in Hair-Follicle-Stem-Cell Leads to IFI16-STING dependent inflammation in Hidradenitis Suppurativa

PROVIDER: PRJNA615650 | ENA |

REPOSITORIES: ENA

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Replication Stress in Hair-Follicle-Stem-Cell Leads to IFI16-STING dependent inflammation in Hidradenitis Suppurativa

Project description:Hidradenitis suppurativa (HS) is a chronic, relapsing, inflammatory skin disease. We characterized hair follicle stem cells isolated from HS and healthy (HD) patients and more precisely the Outer Root Sheath Cells (ORS). We show that transcriptomic analyses of hair follicles from HS (n=6) and HD (n=5) revealed an interferon signature and an alteration of cell cycle pathways

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Project description:Hidradenitis suppurativa (HS) is a severe skin disorder affecting 1% of the global population. Its pathogenesis is multifactorial and poorly understood, involving aberrant keratinization and autoinflammation. Whether autoinflammatory events precede or follow hyperkeratotic changes in hair follicle (HF) epithelia is unknown. Using single-cell RNA sequencing (scRNA-Seq), we defined the cellular composition of HF cells, the primary cells involved in HS, and confirmed these findings in the Fol-HYDRA cohort. We identified three main cell families: i) HF matrix lineage enriched for MSX2, ii) non-matrix lineage enriched for KRT14, and iii) immune cells enriched for PTPRC. Unsupervised clustering of HF cells from controls and HS patients revealed significant differences in non-matrix cells, segregating patients into two groups. Group one is enriched in cluster 1 (IBL), while group two is enriched in cluster 0 (mORS), each displaying distinct transcriptomic changes. Gene set enrichment analysis showed IBLs enriched for keratinization genes and mORS for interferon response genes. Trajectory analysis revealed HF stem cells differentiating into either IBL or mORS pathways. Confirmed in 49 HS patients, these pathways correspond to different clinical phenotypes. Our findings provide a novel perspective on HS pathology, identifying two key pathways: one in keratinization and the other in inflammation. These pathways define different endotypes for HS patients, suggesting potential markers for personalized medicine.

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Hair follicle stem cell replication stress drives IFI16/STING-dependent inflammation in hidradenitis suppurativa.

Project description:Hidradenitis suppurativa (HS) is a chronic, relapsing, inflammatory skin disease. HS appears to be a primary abnormality in the pilosebaceous-apocrine unit. In this work, we characterized hair follicle stem cells (HFSCs) isolated from HS patients and more precisely the outer root sheath cells (ORSCs). We showed that hair follicle cells from HS patients had an increased number of proliferating progenitor cells and lost quiescent stem cells. Remarkably, we also showed that the progression of replication forks was altered in ORSCs from hair follicles of HS patients, leading to activation of the ATR/CHK1 pathway. These alterations were associated with an increased number of micronuclei and with the presence of cytoplasmic ssDNA, leading to the activation of the IFI16/STING pathway and the production of type I IFNs. This mechanistic analysis of the etiology of HS in the HFSC compartment establishes a formal link between genetic predisposition and skin inflammation observed in HS.

| S-EPMC7324185 | biostudies-literature

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