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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression profiling of skin in hidradenitis suppurativa

ABSTRACT: To acquire a better understanding of the molecular pathogenesis of HS, we performed mRNA microarray studies to compare gene expression in lesional skin to healthy skin of HS patients. A significant difference was observed in mRNA expression between lesional and clinically healthy skin of HS patients. Skin biopsy samples (n=30, LS: lesion, NL: non-lesion) were collected at baseline from patients with hidradenitis for RNA extraction and microarray analysis.

ORGANISM(S): Homo sapiens

SUBMITTER: K Li

PROVIDER: E-GEOD-72702 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Gene expression profiling of skin and blood in hidradenitis suppurativa.

Blok J L JL Li K K Brodmerkel C C Jonkman M F MF Horváth B B

The British journal of dermatology 20160302 6

PMID: 26707687

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Molecular profile of hidradenitis suppurativa

Project description:Hidradenitis Suppurativa molecular taxonomy and key signaling pathways were studied by whole transcriptome profiling. Dysregulated genes were detected by comparing lesional and non lesional skin obtained from female HS patients and matched healthy controls using the Agilent array platform

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Project description:The aim of this study was to obtain a better understanding of the molecular background of hidradenitis suppurativa (HS). Global transcriptome analysis of lesional and perilesional skin identifies numerous differentially expressed genes that display unique expression pattern in HS. Genes, whose expression is dysregulated in the skin of patients suffering from HS are novel biomarker candidates and potential therapeutic targets for HS.

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Project description:Molecular taxonomy and key signaling pathways of apocrine glands of patients with hidradenitis suppurativa were studied by whole transcriptome profiling. Dysregulated genes were detected by comparing lesional and non lesional skin obtained from male and female HS patients using the Agilent array platform.

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Pathogenic Keratinocyte States and Fibroblast Niches Define the Tissue Microenvironment in Severe Hidradenitis Suppurativa - Visium

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Pathogenic Keratinocyte States and Fibroblast Niches Define the Tissue Microenvironment in Severe Hidradenitis Suppurativa

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Dynamic Immune-mesenchymal interplay within the tertiary lymphoid structures promotes autoimmune pathogenesis in Hidradenitis Suppurativa

Project description:Tertiary lymphoid structures (TLS) play a pivotal role in sustaining chronic inflammation within autoimmune diseases and tumors by fostering crucial immune cell interactions. While much is known about TLS linked to mucosal epithelium, their formation in the skin epithelium and the supporting microenvironment remains unclear. Using multiomics, we uncovered the presence of TLSs in a severe chronic inflammatory skin disease, Hidradenitis Suppurativa (HS), and showed that lymphocyte proliferation exclusively occurs in TLSs, predominantly located in adjacent to the unique epithelialized tunnels in lesional skin. Notably, we found extensive clonal expansion of plasma cells generating antibodies specific to HS lesional keratinocytes across different patients, alongside the proliferation of Tfh, Treg, and pathogenic T cells (IL17A+ and IFNG+). Additionally, we identified two distinct skin fibroblast populations with transcriptional signatures resembling stromal cells in secondary lymphoid organs (SLO), expressing CXCL13 or CCL19, in response to immune cytokines. Employing a microfluidic system to mimic TLSs-on-a-chip, we demonstrated that HS lesional fibroblasts are critical in orchestrating lymphocyte aggregation and proliferation, which involve TNFα-CXCL13 and TNFα-CCL19 feedback loops with B and T cells, respectively. Furthermore, our study revealed that early TNFα blockade effectively suppresses lymphocyte aggregation, but not after aggregates are formed, underscoring the critical role of TNFα during the initiation of the lymphoid aggregation. Through dissecting the intricate network interactions between immune and mesenchymal cells within the HS lesion, our work revealed the crucial mechanism sustaining chronicity in Hidradenitis Suppurativa and potentially other autoimmune diseases.

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Differentiation Defect Repositions Sebaceous Glands as Instigators in the Early Pathogenesis of Hidradenitis Suppurativa

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Expression data from skin biopsies of Hidradenitis suppurativa patients

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