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A chemogenetic screen for neuroimmune interplay reveals Trpv1+ neuron control of Tregs in the gut [Batch2]

ABSTRACT: Neuroimmune crosstalk participates in intestinal tissue homeostasis and host defense. However, the matrix of interactions between arrays of molecularly-defined neuron subsets and of immunocyte lineages remains unclear. We utilized a chemogenetic approach to activate eight distinct neuronal subsets, assessing effects by deep immunophenotyping, microbiome profiling and immunocyte transcriptomics in intestinal organs. Distinct immune perturbations followed neuronal activation: Nos1+nitrergic neurons regulated Th17-like cells, and Chat+cholinergic neurons regulated neutrophils. Trpv1+ nociceptor neurons elicitinged the broadest immunomodulation, inducing changes in innate lymphocytes, macrophages, and RORγ+ T regulatory (Treg) cells. Further nNeuroanatomical, genetic and pharmacological analysis followup showed that Trpv1+ neurons in dorsal root ganglia decreased Treg cell numbers via the neuropeptide CGRP. Given the role of these neurons in nociception, these data potentially link pain signaling with gut Treg function.

ORGANISM(S): mouse metagenome

PROVIDER: GSE267708 | GEO | 2026/09/01

REPOSITORIES: GEO

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A chemogenetic screen for neuroimmune interplay reveals Trpv1+ neuron control of Tregs in the gut [Batch1]

Project description:Neuroimmune crosstalk participates in intestinal tissue homeostasis and host defense. However, the matrix of interactions between arrays of molecularly-defined neuron subsets and of immunocyte lineages remains unclear. We utilized a chemogenetic approach to activate eight distinct neuronal subsets, assessing effects by deep immunophenotyping, microbiome profiling and immunocyte transcriptomics in intestinal organs. Distinct immune perturbations followed neuronal activation: Nos1+nitrergic neurons regulated Th17-like cells, and Chat+cholinergic neurons regulated neutrophils. Trpv1+ nociceptor neurons elicitinged the broadest immunomodulation, inducing changes in innate lymphocytes, macrophages, and RORγ+ T regulatory (Treg) cells. Further nNeuroanatomical, genetic and pharmacological analysis followup showed that Trpv1+ neurons in dorsal root ganglia decreased Treg cell numbers via the neuropeptide CGRP. Given the role of these neurons in nociception, these data potentially link pain signaling with gut Treg function.

2026-09-01 | GSE267707 | GEO

A chemogenetic screen for neuro-immune interactions in the gut: Trpv1+ nociceptor neurons control T regulatory cells

Project description:Neuroimmune crosstalk is critical for intestinal and tissue homeostasis. Yet the role of molecularly distinct subsets of gut-innervating neurons in regulating the activity of gut immunocytes, and the mechanisms of this neuroimmune signaling remain unclear. Here, we performed a chemogenetic and flow cytometry-based analysis of mice targeting eight different peripheral neuron subsets to assess how gut immunocytes are altered following neural activation. We found that distinct neurons modulated discreet anatomical populations of immunocytes in the gut in ileum, cecum, and colon. Nos1+ neuron activation decreased the percentage of RORg+ ileal conventional CD4+ T cells, whereas ChAT+ neuron activation decreased ileal neutrophils. Trpv1+ neuron activation displayed the most robust immunomodulatory phenotype, causing downregulation of RORg+ T regulatory cells in the colon and cecum. The immune cells exhibited decreased proliferation, enhanced cell stress, and altered cell activation markers. Further genetic and pharmacological approaches showed that spinal afferent Trpv1+ neurons specifically decreased Treg cells by signaling via the neuropeptide CGRP. Our study provided a comprehensive understanding of neuro-immune interactions, revealing a role for mechanisms by which Trpv1+ neurons regulate gut Treg cells.

2024-04-01 | GSE240982 | GEO

The transcriptome of TRPV1-positive sensory neurons revealed by subgroup-elimination transcriptomics

2015-12-30 | E-MTAB-2789 | biostudies-arrayexpress

The transcriptome of TRPV1-positive sensory neurons revealed by subgroup-elimination transcriptomics

Project description:We developed an approach to rapidly eliminate the subgroup of sensory neurons expressing the heat-gated cation channel TRPV1 from dissociated rat sensory ganglia using agonist treatment followed by density centrifugation. To identify transcripts predomintly expressed in TRPV1-positive neurons, we compared the transcriptome of all cells within sensory ganglia versus all cells without TRPV1 expressing neurons using RNA-Seq. Four replicate experiments with RNA from DRG neurons of one rat per experiment were performed. Dissociated neurons were split up in three parts, treated with solvent DMSO (0.1%), casaicin (10 µM), or RTX (100 nM) for 30 min followed by gradient centrifugation. RNA was extracted from the remaining pellet containing either all cells or all cells without TRPV1-positive neurons.

2015-05-12 | E-GEOD-59727 | biostudies-arrayexpress

Distinct nociceptor roles in inflammation and itch revealed by subset-specific transcriptomic adaptation

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

A chemogenetic screen for neuroimmune interplay reveals Trpv1+ neuron control of Tregs in the gut [Batch2]

Project description:A chemogenetic screen for neuroimmune interplay reveals Trpv1+ neuron control of Tregs in the gut [Batch2]

| PRJNA1112438 | ENA

The transcriptome of TRPV1-positive sensory neurons revealed by subgroup-elimination transcriptomics

2015-05-12 | GSE59727 | GEO

The neuronal tyrosine kinase receptor ligand ALKAL2 mediates persistent pain

Project description:To identify putative genes that could contribute to the phenotypic plasticity of TRPV1 nociceptors in inflammation-induced sensitization, we used the Complete Freund’s Adjuvant (CFA) model of chronic inflammatory pain. Three days post intraplantar injection of CFA, ipsilateral and contralateral lumbar DRG neurons were separated, and TRPV1-pHluorin neurons were purified by FACS and analyzed through the GeneChip™ Mouse Gene 2.0 ST Array. The array analysis provided a complete expression profile of mRNA between contralateral and ipsilateral TRPV1 neurons following inflammatory insult. In inflammatory condition, we found >100 genes to be up or down regulated in TRPV1 neurons.

2022-04-22 | GSE201227 | GEO

Engrafted hPSC-Derived Nitrergic Neurons Improve Gut Dysmotility in Mice

Project description:We used bulk RNA-seq to compare gene expression profiles of nitrergic (NO) neurons vs other neurons in control hPSC-derived ENS cultures vs cultures that were enriched in NO nuerons by treating their progenitors with PP121.

2025-06-18 | GSE298676 | GEO

iPSC-derived human sensory neurons reveal a subset of TRPV1 antagonists as anti-pruritic compounds

Project description:Given the inaccessibility of human sensory neurons (SNs), it is yet to be established whether the signalling pathway between histamine 1 receptor (H1R) and transient receptor potential cation channel subfamily V member 1 (TRPV1) is conserved between humans and mammalian models. Accessible human SNs are vital for identifying TRPV1 antagonists with higher potential for success in clinical trials targeting histaminergic itch, especially given TRPV1's species specificity concerns. Hence to build a humanized histamine-dependent itch model, we derived peripheral sensory neurons from human pluripotent stem cells (hiPSC-SNs) and validated channel functionality using immunostaining, calcium imaging and multielectrode array (MEA) recordings. Here, we demonstrated that a subset of hiPSC-SNs exhibits co-expression of H1R and TRPV1, responding to both histamine and capsaicin agonists. We found that inhibiting TRPV1 prevented histamine activation. Moreover, we show that silencing histamine-sensitive neurons reduces capsaicin response, and silencing capsaicin-sensitive neurons diminishes histamine response. To assess the ability of hiPSC-SNs in TRPV1 antagonist drug screening, we evaluated two well-established hyperthermic and three thermal-neutral TRPV1 antagonists. Our finding identifies SB366791, a thermal-neutral antagonist, as a potent inhibitor of H1R activation. The use of hiPSC-SNs may therefore provide a physiologically relevant means to perform large-scale screening to discover anti-pruritic agents predictive of actual efficacy in human clinical trials.

2024-02-27 | GSE256435 | GEO

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