ArticleCellular and molecular gastroenterology and hepatology2018
Communication Between Enteric Neurons, Glia, and Nociceptors Underlies the Effects of Tachykinins on Neuroinflammation.
Article in Cellular and molecular gastroenterology and hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.
- Global research status and trends of enteric glia: a bibliometric analysis.Frontiers in pharmacology · 2024Pooled it
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- Enteric glia, neuropeptides, and Parkinson's: impacts of calcitonin gene-related peptide on gut alpha synuclein.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Enteric nervous system and inflammatory bowel disease.Gastroenterology report · 2026Review
- Enteric nervous system in microbiota-associated gut inflammation.Frontiers in immunology · 2026Review
- Differentiating Enteric Glial Cells Within Intestinal Organoids Derived from Human Pluripotent Stem Cells.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Reviewing the Peripheral and Central Mechanisms of Visceral Hypersensitivity in Intestinal Disorders.International journal of medical sciences · 2026Review
- Gene Therapy in Crohn's Disease: Current Preclinical Challenges and Future Translational Avenues.Biomedicines · 2025Review
- Enteric glia and purinergic signaling in health and disease.Neuropharmacology · 2025Review
- Phosphorylation of Pyruvate Dehydrogenase as a Marker of Neuronal Inactivity in the Enteric Nervous System.Neurogastroenterology and motility · 2025Article
- Enteric glial S100B controls rhythmic colonic functions by regulating excitability and specificity in gut motor neurocircuits.The Journal of physiology · 2025Article
- Purinergic P2YPurinergic signalling · 2025Article
- The role of reactive enteric glia-macrophage interactions in acute and chronic inflammation.Neurogastroenterology and motility · 2025Review
- The role of the enteric nervous system in the pathogenesis of Clostridioides difficile infection.Nature reviews. Gastroenterology & hepatology · 2025Review
- Gut sensory neurons as regulators of neuro-immune-microbial interactions: from molecular mechanisms to precision therapy for IBD/IBS.Journal of neuroinflammation · 2025Review
- Sex Specific Effects of Environmental Toxin-Derived Alpha Synuclein on Enteric Neuronal-Epithelial Interactions.Neurogastroenterology and motility · 2025Article
- Mind the GAPS: Glia associated with psychological stress.Journal of neuroendocrinology · 2025Review
- Gene discovery and pleiotropic architecture of chronic pain in a genome-wide association study of >1.2 million individuals.Research square · 2025Article
- Gene discovery and pleiotropic architecture of Chronic Pain in a Genome-wide Association Study of >1.2 million Individuals.medRxiv : the preprint server for health sciences · 2025Article
24 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Background & Aims: Tachykinins are involved in physiological and pathophysiological mechanisms in the gastrointestinal tract. The major sources of tachykinins in the gut are intrinsic enteric neurons in the enteric nervous system and extrinsic nerve fibers from the dorsal root and vagal ganglia. Although tachykinins are important mediators in the enteric nervous system, how they contribute to neuroinflammation through effects on neurons and glia is not fully understood. Here, we tested the hypothesis that tachykinins contribute to enteric neuroinflammation through mechanisms that involve intercellular neuron-glia signaling. Methods: We used immunohistochemistry and quantitative real-time polymerase chain reaction, and studied cellular activity using transient-receptor potential vanilloid-1 ( Results: Tachykinins are expressed predominantly by intrinsic neuronal varicosities whereas neurokinin-2 receptors (NK2Rs) are expressed predominantly by enteric neurons and TRPV1-positive neuronal varicosities. Stimulation of NK2Rs drives responses in neuronal varicosities that are propagated to enteric glia and neurons. Antagonizing NK2R signaling enhanced recovery from colitis and prevented the development of reactive gliosis, neuroinflammation, and enhanced neuronal contractions. Inflammation drove changes in enteric glial gene expression and function, and antagonizing NK2R signaling mitigated these changes. Neurokinin A-induced neurodegeneration requires glial connexin-43 hemichannel activity. Conclusions: Our results show that tachykinins drive enteric neuroinflammation through a multicellular cascade involving enteric neurons, TRPV1-positive neuronal varicosities, and enteric glia. Therapies targeting components of this pathway could broadly benefit the treatment of dysmotility and pain after acute inflammation in the intestine.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.