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Urotensin II/GPR14 Pathway Regulates Chronic Itch in Mice

ABSTRACT: Urotensin II/GPR14 Pathway Regulates Chronic Itch in Mice

PROVIDER: PRJNA941202 | ENA |

REPOSITORIES: ENA

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Urotensin II/GPR14 Pathway Regulates Chronic Itch in Mice

Project description:In order to analyze the regulatory effects of UII and GPR14 on gene transcription in Mc903-induced atopic dermatitis skin, ear skin collected from MC903 chronic itch mouse model on day 13 was used for in-depth analysis and sequencing of skin gene expression. The effect of GSK1562590 on the expression of pruritus and inflammatory factors in dermatitis was detected by RNA-seq.

2023-06-16 | GSE226669 | GEO

PLAUR-TLR2 Axis Promotes Chronic Itch

Project description:PLAUR-TLR2 Axis Promotes Chronic Itch

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Neuronal BST2: A Pruritic Mediator alongside Protease-Activated Receptor 2 in the IL-27–Driven Itch Pathway

Project description:In the present study, RNA-seq were performed To explore biological significance of IL-27 and BST2 in the neuro-cutaneous signaling network of chronic itch. mRNA profiles were generated by deep sequencing, in triplicate, using MGISEQ-2000. We found that both human keratinocytes and murine sensory neurons responded to IL-27 and BST2, resulting in enrichment of genes promoting itch and inflammation. IL-27-BST2 signaling pathway activation promotes cutaneous inflammation and itch, both leading into an aggravation of AD. This finding might help us to better understand the immune-neuro-modulatory mechanism in itch circuits

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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.

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Estrogen alleviates acute and chronic itch in mice

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PLAUR-TLR2 Axis Promotes Chronic Itch

Project description:In the present study, RNA-seq were performed To identify clinical relevance of PLAUR, a putative Serpin E1 receptor, in cutaneous itch signaling and crosstalk pathways with other critical itch modulators.mRNA profiles were generated by deep sequencing, in triplicate, using MGISEQ-2000. Our experiment showed Serpin E1-treatment further led to a marked upregulation of TLR2 transcript in mDRG neurons, along with enhanced transcription of cosignaling proteins belonging to pro-inflammatory signaling pathways including NF-κB signaling proteins. We next investigated the consequence of TLR2 activation in mTGNs using the TLR agonists, Pam3CSK4 (TLR1/2 agonist), FSL-1 (TLR2/6 agonist), or vehicle. Among these transcripts, TLR2 was found upregulated strongest by both TLR2 agonists suggesting a selfenhancing feedback loop of TLR2 activation.The PLAUR-TLR2 axis promotes cutaneous inflammation and itch, both feeding into an aggravation of AD. This finding might help us to better understand the skin-nerve communication in itch circuits.

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Itch Ubiquitin Ligase Deficiency and B cell LC-MSMS

Project description:The E3 ubiquitin ligase Itch regulates antibody levels and prevents autoimmune disease in humans and mice, yet how Itch regulates B cell fate or function is unknown. We now show that Itch directly limits B cell activity. Using LC-MSMS, we profiled and compared the whole cell proteomes of Itch deficient and Itch sufficient CpG-stimulated B cells. B cells lacking Itch exhibited increased levels of mTORC1 targets and E2F transcription factor targets. These results support a novel role for Itch in limiting B cell metabolism and proliferation.

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Estrogen alleviates acute and chronic itch in mice [exp2]

Project description:Estrogen alleviates acute and chronic itch in mice [exp2]

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Estrogen alleviates acute and chronic itch in mice

Project description:RNAseq analysis showed that estrogen-treatment caused significantly reduced expression level of itch-related molecules

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