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Sensory neuron gene expression changes in response to type 2 skin inflammation

ABSTRACT: Type 2 inflammation contributes to the pathology of skin diseases such as atopic dermatitis and urticaria. Itch is a common symptom accompanying type 2 skin inflammation. Yet how chronic type 2 inflammation affects itch sensory neurons innervating the skin is poorly understood. The goal of this study was to characterize transcriptional changes in sensory ganglia innervating the skin in the setting of chronic type 2 skin inflammation.

ORGANISM(S): Mus musculus

PROVIDER: GSE189542 | GEO | 2025/09/11

REPOSITORIES: GEO

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	GSE189542_RAW.tar	Raw
	GSE189542_all.gene_counts.tsv.gz	Tabular
	filelist.txt	Txt

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Single nuclei RNA and ATAC sequencing of mouse trigeminal ganglia at baseline and in atopic dermatitis-like disease.

Project description:Type 2 inflammation contributes to the pathology of skin diseases such as atopic dermatitis and urticaria. Itch is a common symptom accompanying type 2 skin inflammation. Yet how chronic type 2 inflammation affects itch sensory neurons innervating the skin is poorly understood. The goal of this study was to characterize transcriptional changes in sensory ganglia innervating the skin in the setting of chronic type 2 skin inflammation.

2025-09-11 | GSE190309 | GEO

Sensory neuron gene expression changes in response to type 2 skin inflammation after recovery

Project description:Type 2 inflammation contributes to the pathology of skin diseases such as atopic dermatitis and urticaria. Itch is a common symptom accompanying type 2 skin inflammation. Yet how chronic type 2 inflammation affects itch sensory neurons innervating the skin is poorly understood. The goal of this study was to characterize long term transcriptional changes in sensory ganglia innervating the skin in the setting of chronic type 2 skin inflammation after resolution of inflammation.

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Comparing transcriptional profiles of type 2 innate lymphoid cells from WT and Rag1 knockout mice

Project description:Type 2 inflammation contributes to the pathology of skin diseases such as atopic dermatitis and urticaria. Type 2 innate lymphoid cells are key mediators of skin inflammation by releasing type 2 cytokines in response to certain environmental stimuli. We recently found that Rag1 knockout mice exhibit more pronounced skin inflammation in a mouse model of atopic-dermatitis-like disease, despite lacking adaptive immune cells like T helper 2 cells, implicating a critical role of type 2 innate lymphoid cells in this condition. The goal of this study was to characterize transcriptional differences between WT and Rag KO type 2 innate lymphoid cells to determine if Rag knockout leads to cell-intrinsic alterations in innate lymphoid cell function.

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Proteomics Data of "Integrated Clinical Trial and Molecular Profiling Reveals Immune Drivers of Chronic Hand Eczema" Study

Project description:Background: Chronic hand eczema (CHE) is a debilitating skin condition characterized by pain, itch, and chronic inflammation, with a complex multifactorial origin. Its diverse presentations, including overlapping traits of atopic dermatitis, contact dermatitis, and psoriasis, make diagnosis and treatment particularly challenging. The underlying immune mechanisms of CHE still need to be investigated.Methods: Here we conducted a comprehensive molecular profiling of CHE patients, enrolled without prior selection on etiology and morphology, and performed a phase 2b randomized, multicenter, double-blind, placebo-controlled clinical trial comparing dupilumab to placebo over 16 weeks.Results: We demonstrated that CHE patients may benefit from IL4Rα-blockade, regardless of etiological factors or clinical presentation. Skin transcriptomic and serum profiles of CHE patients closely resemble those seen in both atopic dermatitis and psoriasis, with dysregulated genes affecting keratinocyte differentiation, leucocyte-mediated immunity, cytokine signaling, and mixed type 1, 2, and 3 immunity. The clinical trial included 94 adults with moderate to severe CHE persisting for at least six months and resistant to potent topical corticosteroids. Compared to placebo control, 16-week dupilumab treatment significantly improved clinical severity and quality of life of all CHE patients while largely restoring appropriate transcriptomic and proteomic programs related to skin barrier and immune homeostasis.Conclusion: These findings confirmed the involvement of not only type 2 but also type 1 and type 3 immunity across all CHE patients, and demonstrate that IL-4Rα blockade may offer effective therapeutic perspectives for this highly burdensome condition, independent of an atopic dermatitis background.

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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

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

A sympathetic-basophil axis promotes skin inflammation

Project description:As the largest barrier organ of the body, the skin integrates immune and peripheral sensory nervous systems to respond to environmental stimuli. While sensory neuroimmune interactions in the skin are extensively studied, the role of the sympathetic nervous system (SNS) in skin immunity remains unclear. We show that stress exacerbates atopic dermatitis (AD)-like inflammation in murine models by driving basophil infiltration through SNS activation, independent of the hypothalamic-pituitary-adrenal axis. By elucidating the crosstalk between SNS and inflammation pathways, our study underscores the critical role of autonomic responses in chronic inflammatory skin diseases.

2026-02-10 | GSE288850 | GEO

A sympathetic-basophil axis promotes skin inflammation [Basophil RNA-seq]

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A sympathetic-basophil axis promotes skin inflammation [blood]

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Genome-wide mRNA expression profiling for Wild Type and Itch-/- Skin Transcriptomes by RNA sequencing

Project description:To test the hypothesis that defects in the termination of inflammatory signaling led to skin inflammation that results in the “Itchy” phenotype, we isolated RNA from the lesional skin of Itch-/- mice and from the skin of wild-type mice and performed genome-wide mRNA expression profiling by RNA sequencing. We ranked genes based on the fold change in their expression (increased or decreased) in Itch-/- skin relative to that in wild-type skin. The expression of several TNF–induced genes were increased in Itch-/- skin, including, IL-1?, IL-6, IL-11, IL-19, IL-1RL1, CCL4, CXCL3, CXCL2, CCL3, and CD14. mRNA profiles comparison between wild type (WT) skin and Itch-/- mice lesional skin

2015-03-04 | E-GEOD-65686 | biostudies-arrayexpress

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