ArticleGastroenterology2011
Enteric neuronal density contributes to the severity of intestinal inflammation.
Article in Gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 108 citations in OpenAlex.
- Article
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- Immunological synapse: structures, molecular mechanisms and therapeutic implications in disease.Signal transduction and targeted therapy · 2025Review
- Microbiota in inflammatory bowel disease: mechanisms of disease and therapeutic opportunities.Nature reviews. Microbiology · 2025Review
- Mechanisms of enteric neuropathy in diverse contexts of gastrointestinal dysfunction.Neurogastroenterology and motility · 2025Review
- Neuroimmune interactions: The bridge between inflammatory bowel disease and the gut microbiota.Clinical and translational medicine · 2025Review
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- Sexual dimorphism in colorectal cancer: molecular mechanisms and treatment strategies.Biology of sex differences · 2024Review
- Gastrointestinal Dysmotility Predisposes to Colitis through Regulation of Gut Microbial Composition and Linoleic Acid Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Differences in enteric neuronal density in the NSE-Noggin mouse model across institutes.Scientific reports · 2024Article
- Loss of Baz1b in mice causes perinatal lethality, growth failure, and variable multi-system outcomes.Developmental biology · 2024Article
- Chronic early life stress alters the neuroimmune profile and functioning of the developing zebrafish gut.Brain, behavior, & immunity - health · 2023Article
- Recent developments on BMPs and their antagonists in inflammatory bowel diseases.Cell death discovery · 2023Review
- Serotonergic Control of Gastrointestinal Development, Motility, and Inflammation.Comprehensive Physiology · 2023Article
- Study of tumor necrosis factor receptor in the inflammatory bowel disease.World journal of gastroenterology · 2023Review
- Interstitial Cells of Cajal and Enteric Nervous System in Gastrointestinal and Neurological Pathology, Relation to Oxidative Stress.Current issues in molecular biology · 2023Review
- Review
- Enteric neuroimmune interactions coordinate intestinal responses in health and disease.Mucosal immunology · 2022Review
- The enteric nervous system in gastrointestinal disease etiology.Cellular and molecular life sciences : CMLS · 2021Review
- Acetylcholine ameliorates colitis by promoting IL-10 secretion of monocytic myeloid-derived suppressor cells through the nAChR/ERK pathway.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsEnteric neurons have been reported to be increased in inflamed regions of the bowel in patients with inflammatory bowel disease or intestinal neurogangliomatosis. It is impossible to determine whether this hyperinnervation predates intestinal inflammation, results from it, or contributes to its severity in humans, so we studied this process in mice.
methodsTo determine whether the density of enteric neurons determines the severity of inflammation, we studied transgenic mice that have greater than normal (NSE-noggin mice, which overexpress noggin under the control of the neuron-specific enolase promoter) or fewer than normal (Hand2(+/-) mice) numbers of neurons in the enteric nervous system. Colitis was induced with trinitrobenzene sulfonic acid or dextran sulfate sodium, and the intensity of the resulting inflammation in Hand2(+/-) and NSE-noggin mice was compared with that of wild-type littermates.
resultsSeverity of each form of colitis (based on survival, symptom, and histologic scores; intestinal expression of genes that encode proinflammatory molecules; and levels of neutrophil elastase and p50 nuclear factor κB) were significantly reduced in Hand2(+/-) mice and significantly increased in NSE-noggin animals. Neither mouse differed from wild-type in the severity of delayed-type hypersensitivity (edema, T-cell and neutrophil infiltration, or expression of interleukin-1β, interferon-γ, or tumor necrosis factor-α) induced in the ears using 2,4-dinitro-1-fluorobenzene. Transgene effects on inflammation were therefore restricted to the gastrointestinal tract.
conclusionsThe severity of intestinal inflammation is associated with the density of the enteric innervation in mice. Abnormalities in development of the enteric nervous system might therefore contribute to the pathogenesis of inflammatory bowel disease.
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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.