The intestinal barrier and its regulation by neuroimmune factors: Intestinal barrier and neuroimmune regulation
Abstract
BACKGROUND: The ability to control uptake across the mucosa and protect from damage of harmful substances from the lumen is defined as intestinal barrier function. A disturbed barrier dysfunction has been described in many human diseases and animal models, for example, inflammatory bowel disease, irritable bowel syndrome, and intestinal hypersensitivity. In most diseases and models, alterations are seen both of the paracellular pathway, via the tight junctions, and of the transcellular routes, via different types of endocytosis. Recent studies of pathogenic mechanisms have demonstrated the important role of neuroimmune interaction with the epithelial cells in the regulation of barrier function. Neural impulses from extrinsic vagal and/or sympathetic efferent fibers or intrinsic enteric nerves influence mucosal barrier function via direct effects on epithelial cells or via interaction with immune cells. For example, by nerve-mediated activation by corticotropin-releasing hormone or cholinergic pathways, mucosal mast cells release a range of mediators with effects on transcellular, and/or paracellular permeability (for example, tryptase, TNF-alpha, nerve growth factor, and interleukins). PURPOSE: In this review, we discuss current physiological and pathophysiological aspects of the intestinal barrier and, in particular, its regulation by neuroimmune factors.
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Vagal afferents can respond to histamine, suggesting a route by which microbial-derived histamine may interact with the host nervous system.
“Interestingly vagal afferents can respond to histamine (Keita and Soderholm, 2010), suggesting a route by which microbial-derived histamine may interact with the host nervous system.”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Keita and Soderholm, 2010
In animal models, altered autonomic nervous system activity such as anxiety and stress may play a key role in the pathogenesis of increased intestinal permeability found in the ASD population.
“A further confirmation of the possible central regulation mechanism of the gut-brain axis comes from studies on animal models, where it has been observed that an alteration of autonomic nervous system activity, such as anxiety and stress, could play a key role in the pathogenesis of increased permeability of the intestinal epithelium, found in the ASD population [40,157,158].”
From Autism, Gastrointestinal Symptoms and Modulation of Gut Microbiota by Nutritional Interventions (2019) · cites this paper as [157]
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- Authors
- Keita, Å. V., & Söderholm, J. D.
- Affiliations
- Linköping University (SE)
- Corresponding author
- Söderholm, J. D.
- Venue
- Neurogastroenterology & Motility
- Publisher
- Wiley
- Published
- 2010-02-08
- Volume
- 22
- Issue
- 7
- Pages
- 718-733
- ISSN
- 1350-1925 (ISSN-L)
- 1365-2982
- OpenAlex
- W1564282281
- Cited by
- 286
- References
- 175
- Citations by year
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- FWCI
- 2.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurogastroenterology & Motility (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Keywords
- intestinal barrier function, neuroimmune interactions, tight junctions, paracellular permeability, transcellular permeability, endocytosis, enteric nervous system, vagal innervation, sympathetic innervation, mast cells, corticotropin-releasing factor, cholinergic pathways, inflammatory bowel disease, irritable bowel syndrome, intestinal hypersensitivity, epithelial cells
- MeSH terms
- Animals, Disease Models, Animal, Epithelium, Humans, Intestinal Diseases, Intestinal Mucosa, Intestines, Inflammatory Bowel Diseases, Neuroimmunomodulation, Enteric Nervous System, Neurotransmitter Agents
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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