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HS microbiome

ABSTRACT: The skin microbiome in Hidradenitis Suppurativa

PROVIDER: PRJEB15266 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1607560_1.fastq.gz	Fastqsanger.gz
	ERR1607560_2.fastq.gz	Fastqsanger.gz
	ERR1607570_1.fastq.gz	Fastqsanger.gz
	ERR1607570_2.fastq.gz	Fastqsanger.gz
	ERR1607580_1.fastq.gz	Fastqsanger.gz

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Skin microbiome from hidradenitis suppurativa patients

Project description:Skin microbiome from hidradenitis suppurativa patients

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Project description:Hidradenitis suppurativa (HS) is an inflammatory skin disease with limited therapeutic options. We and others have previously identified an abnormal B cell infiltrate within HS lesional skin. We performed scRNASequencing on CD3 negative cells from inflammatory HS skin lesions, healthy control skin and matched blood to better understand infiltrating B cells amongst other immune cells within lesional skin.

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Project description:This study investigated the underlying inflammatory pathways and cell types in hidradenitis suppurativa using transcriptomic approaches with RNA sequencing of lesional and non-lesional skin biopsies from hidradenitis suppurativa patients.

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Project description:Skin Microbiome in Hidradenitis Suppurativa

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scRNASeq Data of CD45- cells in HS lesional skin and healthy skin

Project description:Hidradenitis suppurativa (HS) is an inflammatory skin disease with limited therapeutic options. Identifying transcriptional alterations within non-immune populations of HS lesions versus healthy controls could identify novel targets for therapy. We profiled subsets sorted as live, CD45 negative cells from biopsies of inflammatory lesions of three patients with HS and six specimens from healthy controls to determine what cell types and pathways were altered in HS inflammatory lesions.

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Project description:Hidradenitis suppurativa is a common, debilitating inflammatory skin disease linked to immune dysregulation and abnormalities in follicular structure and function. Few studies have characterized the transcriptomic profile of affected and unaffected skin. We established an RNA-Seq based hidradenitis suppurativa expression disease signature and found it largely concordant with an earlier microarray-based study. We confirmed known aspects of the underlying disease biology including known immune response pathways, differential regulation of antimicrobial peptides, and complement activation. We further characterize the extent of changes in the complement cascade in hidradenitis lesions and highlight a signature that implicates host response to bacteria in disease pathogenesis.

2020-12-31 | GSE151243 | GEO

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