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IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [scRNAseq]

ABSTRACT: IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [scRNAseq]

PROVIDER: PRJNA961680 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24298917_1.fastq.gz	Fastqsanger.gz
	SRR24298917_2.fastq.gz	Fastqsanger.gz
	SRR24298918_1.fastq.gz	Fastqsanger.gz
	SRR24298918_2.fastq.gz	Fastqsanger.gz
	SRR24298919_1.fastq.gz	Fastqsanger.gz

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IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [scRNAseq]

Project description:The complex system by which the skin regulates immune responses to the external environment is unclear. Here, we investigated cell-cell interactions underlying cutaneous defense against S. aureus. Single-cell transcriptomics (scRNA-Seq) and unbiased network analysis revealed unexpected, dominant IL-17-mediated dermal reticular fibroblast-to-neutrophil communication. Multi-faceted in vitro omics studies demonstrated that IL-17 synergized with several factors including TNF⍺ to induce fibroblast NFKBIZ and chemokine secretion. Cultured fibroblasts drove robust neutrophil recruitment through NFKBIZ-dependent CXCR2 and CXCR4 ligands. Mice lacking IL-17R in fibroblasts (PdgfraΔIl17ra) were generated to determine the significance of fibroblast-neutrophil communication. PdgfraΔIl17ra mice exhibited drastically reduced skin neutrophilia in multiple disease models and reduced defense against S. aureus. These findings were translated to humans by comprehensive analysis of biopsies from psoriasis patients on and off anti-IL-17 treatment. Thus, dermal fibroblasts are critical for skin type 17 inflammation and represent a novel target for treatment of infection and inflammatory disease.

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IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [RNAseq]

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IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense

Project description:IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense

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IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense [RNAseq]

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IL-17 activates dermal reticular fibroblasts to promote neutrophil recruitment and host defense

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CXCL12+ dermal fibroblasts promote neutrophil recruitment and host defense by recognition of IL-17.

Project description:The skin provides an essential barrier for host defense through rapid action of multiple resident and recruited cell types, but the complex communication network governing these processes is incompletely understood. To define these cell-cell interactions more clearly, we performed an unbiased network analysis of mouse skin during invasive S. aureus infection and revealed a dominant role for CXCL12+ fibroblast subsets in neutrophil communication. These subsets predominantly reside in the reticular dermis, express adipocyte lineage markers, detect IL-17 and TNFα, and promote robust neutrophil recruitment through NFKBIZ-dependent release of CXCR2 ligands and CXCL12. Targeted deletion of Il17ra in mouse fibroblasts resulted in greatly reduced neutrophil recruitment and increased infection by S. aureus. Analogous human CXCL12+ fibroblast subsets abundantly express neutrophil chemotactic factors in psoriatic skin that are subsequently decreased upon therapeutic targeting of IL-17. These findings show that CXCL12+ dermal immune acting fibroblast subsets play a critical role in cutaneous neutrophil recruitment and host defense.

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Project description:Neutrophil recruitment is pivotal to host defense against microbial infection, but also contributes to the immunopathology of disease. We investigated the mechanism of neutrophil recruitment in human infectious disease by bioinformatic pathways analysis of the gene expression profiles in the skin lesions of leprosy. In erythema nodosum leprosum (ENL), which occurs in patients with lepromatous leprosy (L-lep), and is characterized by neutrophil infiltration in lesions, the most overrepresented biologic functional group was “cell movement” including E-selectin, which was coordinately regulated with IL-1. In vitro activation of TLR2, upregulated in ENL lesions, triggered induction of IL-1, which together with IFN-, induced E-selectin expression on, and neutrophil adhesion to endothelial cells. Thalidomide, an effective treatment for ENL, inhibited this neutrophil recruitment pathway. The gene expression profile of ENL lesions comprised an integrated pathway of TLR2/FcR activation, neutrophil migration and inflammation, providing insight into mechanisms of neutrophil recruitment in human infectious disease. 6 ENL skin lesions and 7 Lepromatous leprosy skin lesions

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