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Positionally distinct interferon-stimulated dermal immune-acting fibroblasts promote neutrophil recruitment in Sweet’s syndrome [snRNA-seq]

ABSTRACT: Sweet’s syndrome (SS) is a poorly understood inflammatory skin disease. Using RNA sequencing from patients with SS, Pyoderma_Gangrenosum (PG) and healthy controls, in the study, the gaps in the understanding of cellular and molecular landscape of SS and PG skin are addressed.

ORGANISM(S): Homo sapiens

PROVIDER: GSE299795 | GEO | 2025/08/22

REPOSITORIES: GEO

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Positionally distinct interferon-stimulated dermal immune-acting fibroblasts promote neutrophil recruitment in Sweet's syndrome [RNA-seq]

Project description:Sweet’s syndrome is a poorly understood inflammatory skin disease. In this study, cellular and molecular landscape of skin from patients with SS, PG and healthy controls using RNA sequencing have been defined.

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Positionally distinct interferon stimulated dermal immune acting fibroblasts promote neutrophil recruitment in Sweet's syndrome.

Project description:Sweet's syndrome is a poorly understood inflammatory skin disease characterized by neutrophil infiltration to the dermis. Single-nucleus and bulk transcriptomics of archival clinical samples of Sweet's syndrome revealed a prominent interferon signature in Sweet's syndrome skin that was reduced in tissue from other neutrophilic dermatoses. This signature was observed in different subsets of cells, including fibroblasts that expressed interferon-induced genes. Functionally, this response was supported by analysis of cultured primary human dermal fibroblasts that were observed to highly express neutrophil chemokines in response to activation by type I interferon. Furthermore, single-molecule resolution spatial transcriptomics of skin in Sweet's syndrome identified positionally distinct immune acting fibroblasts that included a CXCL1+ subset proximal to neutrophils and a CXCL12+ subset distal to the neutrophilic infiltrate. This study defines the cellular landscape of neutrophilic dermatoses and suggests dermal immune acting fibroblasts play a role in the pathogenesis of Sweet's syndrome through recognition of type I interferons.

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Positionally distinct interferon-stimulated dermal immune-acting fibroblasts promote neutrophil recruitment in Sweet's syndrome [Nanostring CosMx SMI spatial transcriptomics]

Project description:Sweet’s syndrome is a poorly understood inflammatory skin disease characterized by neutrophil infiltration to the dermis. Single-nucleus and bulk transcriptomics of archival clinical samples of Sweet’s syndrome revealed a prominent interferon signature in Sweet’s syndrome skin that was reduced in tissue from another neutrophilic dermatosis, pyoderma gangrenosum, as well as healthy controls. This signature was observed in different subsets of cells, including fibroblasts that expressed interferon-induced genes. Functionally, this response was supported by analysis of cultured primary human dermal fibroblasts that were observed to highly express neutrophil chemokines in response to activation by type I interferon. Furthermore, single-molecule resolution spatial transcriptomics of skin in Sweet’s syndrome identified positionally distinct immune-acting fibroblasts that included a CXCL1+ subset proximal to neutrophils and a CXCL12+ subset distal to the neutrophilic infiltrate. This study defines the cellular landscape of neutrophilic dermatoses and suggests dermal immune-acting fibroblasts play a role in the pathogenesis of Sweet’s syndrome through recognition of type I interferons.

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Positionally distinct interferon-stimulated dermal immune-acting fibroblasts promote neutrophil recruitment in Sweet's syndrome.

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

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

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Project description:The aim of the study was to compare the global transcriptional responses elicited in NHDF cells by three different strains of Borrelia burgdorferi ss (the agent of Lyme borreliosis), representative of different stages in the life cycle of Borrelia: one reference strain isolated from a tick (strain N40), and two invasive strains isolated from skin biopsy of erythema migrans (strain Pbre c4) and acrodermatitis chronica atrophians skin lesions (strain 1408 c1).

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

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