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DNA methylation in Prurigo Nodularis

ABSTRACT: Prurigo nodularis is a debilitating skin condition that is characterized by chronic itch and a prolonged scratching behavior. Little is known of the underlying molecular mechanisms that initiate and maintain the desease. Therefore, we analyzed DNA methylation in prurigo patients and matched healthy controls.

ORGANISM(S): Homo sapiens

PROVIDER: GSE210852 | GEO | 2022/10/31

REPOSITORIES: GEO

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Gene expression Prurigo Nodularis

Project description:Prurigo nodularis is a debilitating skin condition that is characterized by chronic itch and a prolonged scratching behavior. Little is known of the underlying molecular mechanisms that initiate and maintain the desease. Therefore, we analyzed gene expression in prurigo patients and matched healthy controls.

2022-10-31 | GSE210829 | GEO

Treatment-resistant prurigo nodularis: challenges and solutions.

Project description: Not available

| S-EPMC6400231 | biostudies-literature

Prurigo Nodularis

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-10-31 | GSE210854 | GEO

Single-cell RNA sequencing reveals dysregulated fibroblast subclusters in prurigo nodularis

Project description:Prurigo nodularis (PN) is an intensely pruritic, inflammatory skin disease with a poorly understood pathogenesis. Thus, we performed single-cell transcriptomic profiling of 28,695 lesional and non-lesional PN cells. Lesional PN has increased dysregulated fibroblasts (FBs) and myofibroblasts. FBs in lesional PN were shifted towards a cancer-associated fibroblast (CAF)-like phenotype, with POSTN+WNT5A+ CAFs increased in PN, and similarly so in squamous cell carcinoma. A multi-center cohort study revealed an increased risk of SCC and CAF-associated malignancies (breast and colorectal) in PN patients. Systemic fibroproliferative diseases (renal sclerosis and idiopathic pulmonary fibrosis) were upregulated in PN patients. Ligand receptor analyses demonstrated a fibroblast neuronal axis with FB-derived WNT5A and periostin interactions with neuronal receptors MCAM and ITGAV. Compared to atopic dermatitis and psoriasis, mesenchymal dysregulation is unique to PN with an intermediate Th2/Th17 phenotype. These findings identify a pathogenic and targetable POSTN+WNT5A+ fibroblast subpopulation that may predispose CAF-associated malignancies in PN patients.

2024-01-22 | GSE233280 | GEO

Ethnic differences and comorbidities of 909 prurigo nodularis patients.

Project description: Not available

| S-EPMC6518410 | biostudies-literature

Single-cell transcriptome analysis of CD3+ T lymphocytes from prurigo nodularis lesional skin reveals Th17 polarization

Project description:Prurigo nodularis (PN) is a chronic inflammatory skin disease characterized by symmetrically distributed, intensely pruritic nodules of unknown etiology and unmet therapeutic need. The lack of approved therapies and the limited efficacy of off-label treatments reflect the current poor understanding of its pathogenesis. We aimed to comprehensively characterize the phenotypic variation of CD3+ T cells and asses cell-specific gene expression in the lesional skin of patients with PN versus in patients with atopic dermatitis (AD) and in healthy controls (HC). To this end, single-cell RNA sequencing (scRNA-Seq) using 10x Genomics was carried out to compare CD3+ T cells transcriptomic heterogeneity between lesional samples of PN (n=6), AD (n=5) and HC (n=5).

2023-07-08 | GSE213849 | GEO

Single-cell RNA sequencing defines disease-specific differences between chronic nodular prurigo and atopic dermatitis

Project description:Background: Chronic nodular prurigo (CNPG) is a chronic inflammatory skin disease that is maintained by a chronic itch-scratch cycle likely rooted in neuro-immunological dysregulation. This condition may be associated with atopy in some patients, and there are now promising therapeutic results from blocking type-2 cytokines such as IL-4, IL-13 and IL-31. Nevertheless, underlying pathomechanisms as well as the molecular relationship with atopy remain ill-defined. Methods: We profiled skin lesions from patients with CNPG in comparison to atopic dermatitis (AD) and healthy control (HC) individuals using single-cell RNA sequencing combined with T-cell receptor sequencing. Results: We found type-2 immune skewing in both CNPG and AD, as evidenced by CD4+ helper T cells expressing IL13. However, only AD harbored an additional, oligoclonally expanded CD8A+ IL9R+ IL13+ cytotoxic T cell population, and immune activation pathways were highly upregulated in AD, but less so in CNPG. Conversely, CNPG showed signatures of extracellular matrix organization, collagen synthesis, and fibrosis, including a unique population of CXCL14- IL24+ secretory-papillary fibroblasts. Besides known itch mediators such as IL31 and oncostatin M (OSM), we also detected increased levels of neuromedin B (NMB) in fibroblasts of CNPG lesions compared to AD and HC, with NMB receptors detectable on some nerve endings. Conclusion: These data show that CNPG does not harbor the strong disease-specific immune activation pathways that are typically found in AD, but is rather characterized by upregulated stromal remodeling mechanisms that might directly impact itch fibers.

2023-05-24 | GSE222840 | GEO

IL-33-activated calcitonin gene-related peptide-producing memory Th2 cells co-operate with somatosensory neurons to induce conjunctival itch

Project description:Allergic conjunctivitis is a chronic inflammatory disease that is characterized by severe itch in the conjunctiva; but how neuro-immune interactions shape the pathogenesis of severe itch remains unclear. We identified a subset of memory-type pathogenic Th2 cells that preferentially expressed Il1rl1-encoding ST2 and Calca-encoding calcitonin gene-related peptide (CGRP) in the inflammatory conjunctiva using a single-cell analysis. The IL-33-ST2 axis in memory Th2 cells controlled the axonal elongation of the peripheral sensory C-fiber and the induction of severe itch. Pharmacological blockade and genetic deletion of CGRP signaling in vivo attenuated scratching behavior. The analysis of giant papillae from patients with severe allergic conjunctivitis revealed ectopic lymphoid structure formation with the accumulation of IL-33-producing epithelial cells and CGRP-producing pathogenic CD4+ T cells accompanied by peripheral nerve elongation. Thus, the IL-33-ST2-CGRP axis directs severe itch with neuro-reconstruction in the inflammatory conjunctiva and is a potential therapeutic target for severe itch in allergic conjunctivitis.

2022-05-20 | GSE203217 | GEO

Sensory neurons co-opt classical immune signaling pathways to mediate chronic itch

Project description:Mammals have evolved neurophysiologic reflexes such as coughing and scratching to expel invading pathogens and noxious environmental factors. It is well established that these responses are also associated with chronic inflammatory diseases such as asthma and atopic dermatitis. However, the mechanisms by which inflammatory pathways promote sensations such as itch remain poorly understood. Here, we show that the type 2 cytokines IL-4 and IL-13 directly stimulate sensory neurons and that chronic itch is dependent on neuronal IL-4Rα and JAK1 signaling. In proof-of-concept clinical studies, we further show that patients with recalcitrant chronic itch markedly improve when treated with JAK inhibitors. Thus, signaling mechanisms previously ascribed to the immune system may represent novel therapeutic targets within the nervous system. Collectively, these studies reveal an evolutionarily conserved paradigm in which the sensory nervous system employs classical immune signaling pathways to influence mammalian behavior.

2017-09-18 | GSE90883 | GEO

Sensory neurons co-opt classical immune signaling pathways to mediate chronic itch [6 NaV1.8+ Il4raF/F mice treated with MC903 compared to skin from 4 littermates]

Project description:Mammals have evolved neurophysiologic reflexes such as coughing and scratching to expel invading pathogens and noxious environmental factors. It is well established that these responses are also associated with chronic inflammatory diseases such as asthma and atopic dermatitis. However, the mechanisms by which inflammatory pathways promote sensations such as itch remain poorly understood. Here, we show that type 2 cytokines directly stimulate sensory neurons in both mice and humans. Further, we demonstrate that chronic itch is dependent on neuronal IL-4Rα and JAK1 signaling. Based on these observations, we show that patients with recalcitrant chronic itch markedly improve when treated with JAK inhibitors in proof-of-concept clinical studies. Thus, signaling mechanisms previously ascribed to the immune system may represent novel therapeutic targets within the nervous system. Collectively, these studies reveal an evolutionarily conserved paradigm in which the sensory nervous system employs classical immune signaling pathways to influence mammalian behavior.

2017-09-18 | GSE100397 | GEO

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