ArticleNeurogastroenterology and motility2018
Altered gastrointestinal motility involving autoantibodies in the experimental autoimmune encephalomyelitis model of multiple sclerosis.
Article in Neurogastroenterology and motility, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 66 citations in OpenAlex.
- Mechanisms and clinical implications of gut-brain interactions.The Journal of clinical investigation · 2026Review
- Spontaneous enteric nervous system activity generates contractile patterns prior to maturation of gastrointestinal motility.Neurogastroenterology and motility · 2026Article
- Immunization With Bovine Milk Casein Results in Enteric Nervous System Pathology in a Mouse Model of Neuroinflammation.Neurogastroenterology and motility · 2025Article
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- Mechanisms of enteric neuropathy in diverse contexts of gastrointestinal dysfunction.Neurogastroenterology and motility · 2025Review
- Gpr37 modulates the severity of inflammation-induced GI dysmotility by regulating enteric reactive gliosis.iScience · 2025Article
- Association Between Gastrointestinal Symptoms and Disease Severity in Multiple Sclerosis Patients.Cureus · 2025Article
- Article
- Article
- Gut-Brain Interactions and Their Impact on Astrocytes in the Context of Multiple Sclerosis and Beyond.Cells · 2024Review
- Understanding the spectrum of non-motor symptoms in multiple sclerosis: insights from animal models.Neural regeneration research · 2024Review
- Relationship between gut microbiota and multiple sclerosis: a scientometric visual analysis from 2010 to 2023.Frontiers in immunology · 2024Article
- Tryptophan-synthesizing bacteria enhance colonic motility.Neurogastroenterology and motility · 2023Article
- Interaction of the Gut Microbiome and Immunity in Multiple Sclerosis: Impact of Diet and Immune Therapy.International journal of molecular sciences · 2023Review
- Anatomical and functional maturation of the mid-gestation human enteric nervous system.Nature communications · 2023Article
- Loss of ASD-related molecule Cntnap2 affects colonic motility in mice.Frontiers in neuroscience · 2023Article
- Brain-derived neurotrophic factor - a key player in the gastrointestinal system.Przeglad gastroenterologiczny · 2023Review
- A review of the auditory-gut-brain axis.Frontiers in neuroscience · 2023Review
- Impact of Siponimod on Enteric and Central Nervous System Pathology in Late-Stage Experimental Autoimmune Encephalomyelitis.International journal of molecular sciences · 2022Article
- The Crosstalk between Vitamin D and Pediatric Digestive Disorders.Diagnostics (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMultiple sclerosis (MS) is an autoimmune disease of the central nervous system that, in addition to motor, sensory, and cognitive symptoms, also causes constipation, which is poorly understood. Here, we characterize gastrointestinal (GI) dysmotility in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS and evaluate whether autoantibodies target the enteric nervous system (ENS) and cause dysmotility.
methodsEAE was induced in male SJL and B6 mice. GI motility was assessed in vivo and ex vivo in wild type (WT) and B cell-deficient mice. MS and EAE serum was used to survey potential targets in the ENS and changes in the ENS structure were characterized using immunohistochemistry. KEY
resultsEAE mice developed accelerated gastric emptying and delayed whole GI transit with reduced colonic motility. Fecal water content was reduced, and colonic migrating myoelectrical complexes (CMMC) and slow waves were less frequent. Colons from EAE mice exhibited decreased GFAP levels in glia. Sera from MS patients and from EAE mice targeted ENS neurons and glia. B-cell deficiency in EAE protected against colonic dysmotility. CONCLUSIONS & INFERENCES: Consistent with symptoms experienced in MS, we demonstrate that EAE mice widely exhibit features of GI dysmotility that persisted in the absence of extrinsic innervation, suggesting direct involvement of ENS neurocircuitry. The absence of GI dysmotility in B cell-deficient mice with EAE together with EAE and MS serum immunoreactivity against ENS targets suggests that MS could be classified among other diseases known to induce autoimmune GI dysmotility.
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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.