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Effects of PDGFRa-lineage leukocyte extravasation to skin in atopic dermatitis

ABSTRACT: Effects of PDGFRa-lineage leukocyte extravasation to skin in atopic dermatitis

PROVIDER: PRJNA702124 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13721816_1.fastq.gz	Fastqsanger.gz
	SRR13721816_2.fastq.gz	Fastqsanger.gz
	SRR13721817_1.fastq.gz	Fastqsanger.gz
	SRR13721817_2.fastq.gz	Fastqsanger.gz
	SRR13721818_1.fastq.gz	Fastqsanger.gz

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Effects of PDGFRa-lineage leukocyte extravasation to skin in atopic dermatitis

Project description:The circulating leukocyte population contains a fraction of cells derived from progenitors that had transient PDGFRa expression during embryonic development (PDGFRa-lineage). During inflammation, extravasated leukocytes in inflamed tissue modify the tissue-resident leukocyte population and crosstalk with the stromal cells. The current study investigates the effects of extravasated leukocytes derived from PDGFRa-lineage origin on the skin in atopic dermatitis (AD). Lineage- bone marrow progenitors were isolated from PDGFRa-lineage labeling mice which labels cells derived from PDGFRa-lineage with tdTomato. Progenitors derived from PDGFRa-lineage or non-PDGFRa-lineage were transplanted to irradiated EGFP-transgenic mice and allowed for bone marrow reconstitution (BMT). AD was then induced by repeated topical application of MC903 for six times. On day 14, RNA was isolated from inflamed skin to construct library for bulk RNA sequencing. AD skin transcriptomes of PDGFRa-lineage and non-PDGFRa-lineage BMTs were compared. In addition, the obtained dataset were paired with flow cytometric measurement of leukocyte extravasation to compare samples with similar extravasation loads. We found via functional enrichment analyses that extravasated PDGFRa-lineage leukocytes possess intrinsic properties that differ from non-PDGFRa-lineage, coordinate stronger inflammatory responses and modulate the extracellular matrix.

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Project description:Clinical overlaps between psoriasis and atopic dermatitis are sometimes undiscernible, and there is no consensus whether to treat the overlap phenotype as psoriasis or atopic dermatitis. We enrolled patients diagnosed with either psoriasis or atopic dermatitis, and clinically re-stratified them into classic psoriasis, classic atopic dermatitis, and the overlap phenotype between psoriasis and atopic dermatitis. We compared gene expression profiles of lesional and nonlesional skin biopsy tissues between the three comparison groups. Global mRNA expression and T-cell subset cytokine expression in the skin of the overlap phenotype were consistent with the profiles of psoriasis and different from the profiles of atopic dermatitis. Unsupervised k-means clustering indicated that the best number of distinct clusters for the total population of the three comparison groups was two, and the two clusters of psoriasis and atopic dermatitis were differentiated by gene expression. Our study suggests that clinical overlap phenotype between psoriasis and atopic dermatitis has dominant molecular features of psoriasis, and genomic biomarkers can differentiate psoriasis and atopic dermatitis at molecular levels in patients with a spectrum of psoriasis and atopic dermatitis.

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