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NF-kB Perturbation Reveals Unique Immunomodulatory Functions in Prx1+ Fibroblasts that Promote Atopic Dermatitis

ABSTRACT: NF-kB Perturbation Reveals Unique Immunomodulatory Functions in Prx1+ Fibroblasts that Promote Atopic Dermatitis

PROVIDER: PRJNA722491 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14253412.fastq.gz	Fastqsanger.gz
	SRR14253413.fastq.gz	Fastqsanger.gz
	SRR14253414.fastq.gz	Fastqsanger.gz
	SRR14253415.fastq.gz	Fastqsanger.gz
	SRR14253416.fastq.gz	Fastqsanger.gz

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NF-kB Perturbation Reveals Unique Immunomodulatory Functions in Prx1+ Fibroblasts that Promote Atopic Dermatitis

Project description:Skin is composed of diverse cell populations that cooperatively maintain homeostasis. Upregulation of the NF-kB pathway may lead to the development of chronic inflammatory disorders of the skin, but the early events in situ are not well understood. Through analysis of single cell RNA sequencing (scRNA-seq) data via iterative Random Forest Leave One Out Prediction (iRF-LOOP), an explainable artificial intelligence (X-AI) method, we identified an immunoregulatory role for a unique Prx1+ fibroblast subpopulation. Disruption of Ikkb/NFkB under homeostatic conditions in these fibroblasts paradoxically induced skin inflammation due to the over-expression of CCL11 (eotaxin-1) characterized by eosinophil infiltration and a subsequent Th2 immune response. Because the inflammatory phenotype resembled that seen in human atopic dermatitis (AD), we examined validated human AD skin samples and found that human AD fibroblasts also over-expressed CCL11 compared to control skin. Importantly, we demonstrate that monoclonal antibody treatment against CCL11 was therapeutically effective in reducing the eosinophilia and Th2 inflammation in vivo. Taken together, the murine model and human AD specimens point to dysregulated Prx1+ fibroblasts as a previously unrecognized etiologic factor that may contribute to the pathogenesis of AD-like lesions and suggest targeting CCL11 as a novel way to treat AD-like lesions.

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Project description:Skin is composed of diverse cell populations that cooperatively maintain homeostasis. Up-regulation of the nuclear factor κB (NF-κB) pathway may lead to the development of chronic inflammatory disorders of the skin, but its role during the early events remains unclear. Through analysis of single-cell RNA sequencing data via iterative random forest leave one out prediction, an explainable artificial intelligence method, we identified an immunoregulatory role for a unique paired related homeobox-1 (Prx1)+ fibroblast subpopulation. Disruption of Ikkb-NF-κB under homeostatic conditions in these fibroblasts paradoxically induced skin inflammation due to the overexpression of C-C motif chemokine ligand 11 (CCL11; or eotaxin-1) characterized by eosinophil infiltration and a subsequent TH2 immune response. Because the inflammatory phenotype resembled that seen in human atopic dermatitis (AD), we examined human AD skin samples and found that human AD fibroblasts also overexpressed CCL11 and that perturbation of Ikkb-NF-κB in primary human dermal fibroblasts up-regulated CCL11. Monoclonal antibody treatment against CCL11 was effective in reducing the eosinophilia and TH2 inflammation in a mouse model. Together, the murine model and human AD specimens point to dysregulated Prx1+ fibroblasts as a previously unrecognized etiologic factor that may contribute to the pathogenesis of AD and suggest that targeting CCL11 may be a way to treat AD-like skin lesions.

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