The Similarity and Difference: Response and Molecular Characteristics of Peripheral Sensory Neurons Associated to Pain and Itch
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ABSTRACT:
PROVIDER: PRJNA1130417 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29664314_1.fastq.gz | Fastqsanger.gz | |||
| SRR29664314_2.fastq.gz | Fastqsanger.gz | |||
| SRR29664315_1.fastq.gz | Fastqsanger.gz | |||
| SRR29664315_2.fastq.gz | Fastqsanger.gz | |||
| SRR29664316_1.fastq.gz | Fastqsanger.gz |
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Project description:The dorsal root ganglion (DRG) neurons take in charge of primary detection and transmission of peripheral pain and itch stimuli, however, as two distinct noxious sensation, it is still attractive for this field that how the DRG neurons differentially response and code pain and itch. Here, we investigate the response and activation spectrum of DRG neurons under peripheral pain and itch stimuli using in vivo two-photon calcium imaging, and find differences in the responsive intensity to pain and itch between multisensory neurons (both pain and itch) and single-sensory neurons (either pain or itch). Besides, single-cell RNA sequencing (scRNA-seq) is used to reveal the heterogeneity of distinct subpopulations based on their expression of pain- or itch-related marker genes and indicates the similarity and difference of their transcriptomic changes under chronic pain and itch. Our results will provide fundamental insights to the peripheral pain and itch differential coding mechanism, moreover, benefit the development of pain and itch therapies.
2024-11-20 | GSE271186 | GEO
Project description:In order to study the effect of UII on the transcription level regulation of itch-related genes in sensory neurons and keratinocytes, and to apply UII in mouse dorsal root ganglion neuronal cells and keratinocytes, the study showed that UII significantly upregulated the expression of various characteristics of atopic dermatitis and itch-related genes, such as Fasl, Mrgprx1, Amy2a3, INHBA, IL36G, STEAP2, etc.
2025-11-23 | GSE218749 | GEO
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
Project description:Itch is an unpleasant skin sensation which can be triggered by exposure to many chemicals including those released by mast cells. The Nppb-expressing class of sensory neurons when activated elicit scratching responses in mice, however, it is unclear which itch-inducing agents stimulate these cells and the receptors involved. Here, we identify receptors expressed by Nppb-neurons and demonstrate the functional importance of these receptors as sensors of endogenous pruritogens released by mast cells. Our search for receptors in Nppb-neurons revealed that they express leukotriene, serotonin, and sphingosine-1-phosphate receptors. Targeted cell ablation, calcium imaging of primary sensory neurons, and conditional receptor knockout studies demonstrate that these receptors induce itch by the direct stimulation of Nppb-neurons and neurotransmission through the canonical GRP-dependent spinal cord itch pathway. Together our results define a molecular and cellular pathway for mast cell-induced itch.
2019-03-26 | GSE125626 | GEO
Project description:Background: Anti-type 2 cytokine therapies represent promising interventions for chronic itch; however, their precise mechanisms in restoring nerve architecture and mitigating inflammation and pruritus remain incompletely understood. This study aimed to elucidate the mechanistic roles of IL-4, IL-13, and IL-31 in the pathophysiology of itch associated with type 2 inflammatory skin diseases. Methods: The effect of IL-4, IL-13, and/or IL-31 on neurite outgrowth and/or transcriptomic changes were analyzed in human and mouse dorsal root ganglion (DRG) neuronal cultures. Mouse ear pinnae were processed for histologic, transcriptomic, and proteomic analyses 4 days after intradermal injection of IL-4, IL-13, and/or IL-31. To evaluate functional correlations with neuronal responses, mice were subcutaneously challenged with IL-4, IL-13, and/or IL-31, and scratching behavior was monitored. Association between IL-4/IL-13–IL-4Rα axis and severity of atopic dermatitis (AD) was evaluated through correlative analyses of human DRG transcriptomic changes and AD transcriptomic datasets (GSE130588 and BioMap consortium). Results: IL-4 and IL-13 promote mouse and human DRG sensory neuron growth, with effects similar to or greater than IL-31. In mice, intradermal IL-4, IL-13, and IL-31 increased epidermal nerve growth; however, only IL-4 and IL-13 induced hyperplasia and immune cell recruitment. Multi-omic analyses revealed that IL-4 and IL-13 have a broader impact on neuroimmune interactions than IL-31. In a murine DRG neuron-eosinophil co-culture, IL-4Rα blockade reduced neurite growth. IL-13 and IL-31 elicited acute scratching, demonstrating their roles as direct pruritogens; IL-4 synergistically enhanced IL-13-induced itch, resulting in greater pruritic responses than IL-31. Additionally, a set of itch-associated genes upregulated by IL-4 and IL-13 and downregulated by dupilumab-mediated IL-4Rα blockade in human DRG neuronal cultures showed positive correlation with AD severity. Conclusions: These findings establish the IL-4/IL-13–IL-4Rα axis as a key regulator of inflammatory skin nerve innervation, neuroimmune interactions, barrier integrity, and itch response, highlighting its mechanistic role in modulating sensory neuronal function and shaping the inflammatory microenvironment that drives itch pathophysiology.
2025-05-15 | GSE296776 | GEO
Project description:Background: Anti-type 2 cytokine therapies represent promising interventions for chronic itch; however, their precise mechanisms in restoring nerve architecture and mitigating inflammation and pruritus remain incompletely understood. This study aimed to elucidate the mechanistic roles of IL-4, IL-13, and IL-31 in the pathophysiology of itch associated with type 2 inflammatory skin diseases. Methods: The effect of IL-4, IL-13, and/or IL-31 on neurite outgrowth and/or transcriptomic changes were analyzed in human and mouse dorsal root ganglion (DRG) neuronal cultures. Mouse ear pinnae were processed for histologic, transcriptomic, and proteomic analyses 4 days after intradermal injection of IL-4, IL-13, and/or IL-31. To evaluate functional correlations with neuronal responses, mice were subcutaneously challenged with IL-4, IL-13, and/or IL-31, and scratching behavior was monitored. Association between IL-4/IL-13–IL-4Rα axis and severity of atopic dermatitis (AD) was evaluated through correlative analyses of human DRG transcriptomic changes and AD transcriptomic datasets (GSE130588 and BioMap consortium). Results: IL-4 and IL-13 promote mouse and human DRG sensory neuron growth, with effects similar to or greater than IL-31. In mice, intradermal IL-4, IL-13, and IL-31 increased epidermal nerve growth; however, only IL-4 and IL-13 induced hyperplasia and immune cell recruitment. Multi-omic analyses revealed that IL-4 and IL-13 have a broader impact on neuroimmune interactions than IL-31. In a murine DRG neuron-eosinophil co-culture, IL-4Rα blockade reduced neurite growth. IL-13 and IL-31 elicited acute scratching, demonstrating their roles as direct pruritogens; IL-4 synergistically enhanced IL-13-induced itch, resulting in greater pruritic responses than IL-31. Additionally, a set of itch-associated genes upregulated by IL-4 and IL-13 and downregulated by dupilumab-mediated IL-4Rα blockade in human DRG neuronal cultures showed positive correlation with AD severity. Conclusions: These findings establish the IL-4/IL-13–IL-4Rα axis as a key regulator of inflammatory skin nerve innervation, neuroimmune interactions, barrier integrity, and itch response, highlighting its mechanistic role in modulating sensory neuronal function and shaping the inflammatory microenvironment that drives itch pathophysiology.
2025-05-15 | GSE296778 | GEO
Project description:Distinct representation of visceral pain and itch by unique BLA neuronal ensembles and suggested that BLA as a sorting center that distinctly processes visceral pain and itch, providing a new framework for comprehending how the brain processes nociceptive and pruritus information, and identifying potential molecular targets for specific visceral pain and itch processing.
2026-05-01 | GSE296186 | GEO
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
Project description:Urotensin II Activates Sensory-cutaneous Pathway to Promote Itch and Cutaneous Inflammation
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Project description:This study identifies two distinct subsets of sensory neurons that separately regulate itch and inflammation in allergic contact dermatitis. MrgprD⁺ nonpeptidergic neurons adopt a transient regenerative program during inflammation and are essential for itch behavior, while Trpv1⁺ peptidergic neurons limit inflammation by restraining neutrophil infiltration. These findings uncover parallel, nonredundant neuronal circuits that independently control inflammatory and pruritic responses in the skin.
2026-04-15 | GSE315295 | GEO