ArticleInflammatory bowel diseases2013
Tumor necrosis factor-neuropeptide Y cross talk regulates inflammation, epithelial barrier functions, and colonic motility.
Article in Inflammatory bowel diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 61 citations in OpenAlex.
- A biomechanical model of inflammation-driven colon hypertrophy and dysmotility: Application to Gulf War Illness.Journal of the mechanical behavior of biomedical materials · 2026Article
- Animal Models of Slow-Transit Constipation: Current Progress, Limitations, and Future Perspectives.Digestive diseases and sciences · 2026Review
- Neuroimmune Interactions in Inflammatory Skin and Intestinal Diseases.Journal of inflammation research · 2026Review
- Coordinated regulation of colonic fluid and mucus secretion.Frontiers in pharmacology · 2026Review
- Neuropeptide Y Boosts Intestinal Mucosal Immunity of Tilapia Infected withAnimals : an open access journal from MDPI · 2025Article
- Rapamycin reveals neuropeptide Y as a regulator of senescence and inflammatory pathways in arthritis.Neuropeptides · 2025Article
- Skin Resident T Cell Interactions with NPY1RbioRxiv : the preprint server for biology · 2025Article
- Hawthorn Vinegar in Health with a Focus on Immune Responses.Nutrients · 2024Article
- Study of tumor necrosis factor receptor in the inflammatory bowel disease.World journal of gastroenterology · 2023Review
- Gut region-specific TNFR expression: TNFR2 is more affected than TNFR1 in duodenal myenteric ganglia of diabetic rats.World journal of diabetes · 2023Article
- Soluble TNF mediates amyloid-independent, diet-induced alterations to immune and neuronal functions in an Alzheimer's disease mouse model.Frontiers in cellular neuroscience · 2023Article
- Recent insights of obesity-induced gut and adipose tissue dysbiosis in type 2 diabetes.Frontiers in molecular biosciences · 2023Review
- Guardians of the gut: influence of the enteric nervous system on the intestinal epithelial barrier.Frontiers in medicine · 2023Review
- Review
- Neonatal development of intestinal neuroimmune interactions.Trends in neurosciences · 2022Review
- The Role of Inflammatory Mediators in the Development of Gastrointestinal Motility Disorders.International journal of molecular sciences · 2022Review
- Opioid Use, Gut Dysbiosis, Inflammation, and the Nervous System.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2022Review
- Intracolonic Neuropeptide Y Y1 Receptor Inhibition Attenuates Intestinal Inflammation in Murine Colitis and Cytokine Release in IBD Biopsies.Inflammatory bowel diseases · 2022Article
- LPAR1 regulates enteric nervous system function through glial signaling and contributes to chronic intestinal pseudo-obstruction.The Journal of clinical investigation · 2022Article
- The Regulation of Phoenixin: A Fascinating Multidimensional Peptide.Journal of the Endocrine Society · 2022Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundNeuro-immune interactions play a significant role in regulating the severity of inflammation. Our previous work demonstrated that neuropeptide Y (NPY) is upregulated in the enteric nervous system during murine colitis and that NPY knockout mice exhibit reduced inflammation. Here, we investigated if NPY expression during inflammation is induced by tumor necrosis factor (TNF), the main proinflammatory cytokine.
methodsUsing primary enteric neurons and colon explant cultures from wild type and NPY knockout (NPY(-/-)) mice, we determined if NPY knockdown modulates TNF release and epithelial permeability. Further, we assessed if NPY expression is inducible by TNF in enteric neuronal cells and mouse model of experimental colitis, using the TNF inhibitors-etanercept (blocks transmembrane and soluble TNF) and XPro1595 (blocks soluble TNF only).
resultsWe found that enteric neurons express TNF receptors (TNFR1 and R2). Primary enteric neurons from NPY(-/-) mice produced less TNF compared with wild type. Further, TNF activated NPY promoter in enteric neurons through phospho-c-Jun. NPY(-/-) mice had decreased intestinal permeability. In vitro, NPY increased epithelial permeability through phosphatidyl inositol-3-kinase (PI3-K)-induced pore-forming claudin-2. TNF inhibitors attenuated NPY expression in vitro and in vivo. TNF inhibitor-treated colitic mice exhibited reduced NPY expression and inflammation, reduced oxidative stress, enhanced neuronal survival, and improved colonic motility. XPro1595 had more protective effects on neuronal survival and motility compared with etanercept.
conclusionsWe demonstrate a novel TNF-NPY cross talk that modulates inflammation, barrier functions, and colonic motility during inflammation. It is also suggested that selective blocking of soluble TNF may be a better therapeutic option than using anti-TNF antibodies.
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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.