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Inflammasome activation drives inflammation in hidradenitis suppurativa skin

ABSTRACT: Inflammasome activation drives inflammation in hidradenitis suppurativa skin

PROVIDER: PRJNA876946 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21426100_1.fastq.gz	Fastqsanger.gz
	SRR21426100_2.fastq.gz	Fastqsanger.gz
	SRR21426101_1.fastq.gz	Fastqsanger.gz
	SRR21426101_2.fastq.gz	Fastqsanger.gz
	SRR21426102_1.fastq.gz	Fastqsanger.gz

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Inflammasome activation drives inflammation in hidradenitis suppurativa skin

Project description:Treatment for the debilitating, chronic skin disease hidradenitis suppurativa (HS) is grossly inadequate. A better understanding of its pathogenesis is required to design new therapeutic strategies. Despite an incidence of approximately 1 in 200, HS is underrecognized and underdiagnosed, with a high morbidity and poor quality of life, which may last decades. In this study we first employed single cell RNA sequencing to analyse gene expression in immune cells isolated from HS lesions compared with healthy control skin. We identified 30 unique immune cell clusters, with a significant enrichment in the frequency of plasma cells, Th17 cells and a subset of dendritic cells (DC) in HS skin. These findings were validated by flow cytometry, which revealed a significant increase in infiltrating immune cells in HS skin, including T cells, B cells, neutrophils, dermal macrophages and DC. The sequencing analysis revealed that the immune transcriptome in HS skin was distinct and much more heterogenous, when compared with healthy skin. Genes and pathways associated with Th17 cells and IL-17, IL-1β, and the NLRP3 inflammasome were enhanced in HS skin, particularly in samples with a high inflammatory load. Inflammasome constituent genes principally mapped to Langerhans cells and a subpopulation of DC. A skin explant model showed that culture of HS skin with an NLRP3 inflammasome inhibitor reduced the inflammatory response, with significant reduction of IL-1β and IL-17A as well as other key mediators of inflammation. These data provide a rationale for targeting the IL-17 pathway in HS, particularly upstream at the NLRP3 inflammasome.

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