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Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE292635 | GEO | 2025/06/25

REPOSITORIES: GEO

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Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense [RNA-Seq]

Project description:Enteric nervous system (ENS)-derived neuropeptides modulate immune cell function, yet our understanding of how inflammatory cues directly influence enteric neuron responses during infection is considerably lacking. Here, we characterize a primary enteric sensory neuron (PSN) subset that produces the neuropeptides neuromedin U (NMU) and calcitonin gene-related peptide beta (CGRPβ) and co-expresses receptors for the type 2 cytokines IL-4 and IL-13. Type 2 cytokines were sufficient to upregulate NMU and CGRPβ expression in PSNs, in vitro and in vivo, which was abrogated by PSN-specific Il13ra1 deletion. Importantly, PSN-specific Il13ra1 deletion impaired host defense to the gastrointestinal helminth H. polygyrus, diminished enteric sensory neuron populations, and blunted muscularis immune responses. Co-administration of NMU23 and CGRPβ rescued helminth clearance deficits and restored anti-helminth immunity. Mechanistically, we show that CGRPβ signaling synergizes with IL-4 in intestinal macrophages, inducing alternatively-activated macrophage defense responses, altogether illustrating the critical role of bi-directional neuro-immune crosstalk in regulating intestinal type 2 immunity.

2025-06-25 | GSE292633 | GEO

Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense [scRNA-Seq]

2025-06-25 | GSE292613 | GEO

Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense [RNA-Seq 2]

2025-06-25 | GSE292634 | GEO

Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense

Project description:Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense

| PRJNA1240342 | ENA

Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense [RNA-Seq]

Project description:Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense [RNA-Seq]

| PRJNA1240348 | ENA

Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense [scRNA-Seq]

Project description:Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense [scRNA-Seq]

| PRJNA1240301 | ENA

Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense [RNA-Seq 2]

Project description:Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense [RNA-Seq 2]

| PRJNA1240347 | ENA

Sensory Nociceptive Neurons Contribute to Host Protection During Enteric Infection With Citrobacter rodentium.

Project description:BackgroundNeurons are an integral component of the immune system that functions to coordinate responses to bacterial pathogens. Sensory nociceptive neurons that can detect bacterial pathogens are found throughout the body with dense innervation of the intestinal tract.MethodsIn this study, we assessed the role of these nerves in the coordination of host defenses to Citrobacter rodentium. Selective ablation of nociceptive neurons significantly increased bacterial burden 10 days postinfection and delayed pathogen clearance.ResultsBecause the sensory neuropeptide CGRP (calcitonin gene-related peptide) regulates host responses during infection of the skin, lung, and small intestine, we assessed the role of CGRP receptor signaling during C rodentium infection. Although CGRP receptor blockade reduced certain proinflammatory gene expression, bacterial burden and Il-22 expression was unaffected.ConclusionsOur data highlight that sensory nociceptive neurons exert a significant host protective role during C rodentium infection, independent of CGRP receptor signaling.

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Cytokines reprogram airway sensory neurons in asthma.

Project description:Nociceptor neurons play a crucial role in maintaining the body's homeostasis by detecting and responding to potential dangers in the environment. However, this function can be detrimental during allergic reactions, since vagal nociceptors can contribute to immune cell infiltration, bronchial hypersensitivity, and mucus imbalance, in addition to causing pain and coughing. Despite this, the specific mechanisms by which nociceptors acquire pro-inflammatory characteristics during allergic reactions are not yet fully understood. In this study, we aimed to investigate the molecular profile of airway nociceptor neurons during allergic airway inflammation and identify the signals driving such reprogramming. Using retrograde tracing and lineage reporting, we identified a unique class of inflammatory vagal nociceptor neurons that exclusively innervate the airways. In the ovalbumin mouse model of airway inflammation, these neurons undergo significant reprogramming characterized by the upregulation of the NPY receptor Npy1r. A screening of cytokines and neurotrophins revealed that IL-1β, IL-13 and BDNF drive part of this reprogramming. IL-13 triggered Npy1r overexpression in nociceptors via the JAK/STAT6 pathway. In parallel, sympathetic neurons and macrophages release NPY in the bronchoalveolar fluid of asthmatic mice, which limits the excitability of nociceptor neurons. Single-cell RNA sequencing of lung immune cells has revealed that a cell-specific knockout of Npy1r in nociceptor neurons in asthmatic mice leads to an increase in airway inflammation mediated by T cells. Opposite findings were observed in asthmatic mice in which nociceptor neurons were chemically ablated. In summary, allergic airway inflammation reprograms airway nociceptor neurons to acquire a pro-inflammatory phenotype, while a compensatory mechanism involving NPY1R limits nociceptor neurons' activity.

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Cytokines in innate host defense in the lung.

Project description: Not available

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