Evidence map›Paper›PMID 16931576›Full record

ArticleGut2007

Ileitis alters neuronal and enteroendocrine signalling in guinea pig distal colon.

Jennifer R O'Hara, Alan E Lomax, Gary M Mawe, Keith A Sharkey

Open access · bronzeAbstract read
In one paragraph

Article in Gut, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  15. Recent advances in small bowel diseases: Part II.World journal of gastroenterology · 2012
    Review
  16. Article
  17. Neuroinflammation in inflammatory bowel disease.Journal of neuroinflammation · 2010
    Review
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Jennifer R O'HaraDepartment of Physiology and Biophysics, University of Calgary, 3330 Hospital Dr. NW, Calgary, Alberta T2N 4N1, Canada.
Alan E Lomax
Gary M Mawe
Keith A Sharkey
University of Calgary · CAUniversity of Vermont · US

Funding

Neuronal Excitability and Motility in ColitisR01DK062267 · NIDDK · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI MAWE, GARY M · 2002 to 2016
$3.3M
NIDDK NIH HHS DK62267NIDDK NIH HHS R01 DK062267
6 · The paper itself

Abstract

BACKGROUND AND

aimsIntestinal inflammation alters neuronal and enteroendocrine signalling, leading to functional adaptations in the inflamed bowel. Human studies have reported functional alterations at sites distant from active inflammation. Our aims were to determine whether neuronal and enteroendocrine signalling are altered in the uninflamed colon during ileitis.

methodsWe used neurophysiological, immunohistochemical, biochemical and Ussing chamber techniques to examine the effect of 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced ileitis on the properties of submucosal neurones, enteroendocrine cells and epithelial physiology of the distal colon of guinea pigs.

resultsThree days after TNBS administration, when inflammation was restricted to the ileum, the properties of colonic enteric neurones were altered. Submucosal AH neurones were hyperexcitable and had reduced after hyperpolarisations. S neurones received larger fast and slow excitatory postsynaptic potentials, due to an increase in non-cholinergic synaptic transmission. Despite the absence of inflammation in the colon, we found increased colonic prostaglandin E(2) content in animals with ileitis. Ileitis also increased the number of colonic 5-hydroxytryptamine (5-HT)- and GLP-2-immunoreactive enteroendocrine cells. This was accompanied by an increase in stimulated 5-HT release. Functional alterations in epithelial physiology occurred such that basal short circuit current was increased and veratridine-stimulated ion transport was reduced in the colon of animals with ileitis.

conclusionOur data suggest that inflammation at one site in the gut alters the cellular components of enteric reflex circuits in non-inflamed regions in ways similar to those at sites of active inflammation. These changes underlie altered function in non-involved regions during episodes of intestinal inflammation.

Indexed as

AnimalsBethanecholCell CountColforsinColonDinoprostoneEnteroendocrine CellsEpithelial CellsExcitatory Postsynaptic PotentialsGuinea PigsIleitisIntestinal MucosaIon TransportMaleMotor NeuronsMuscarinic AgonistsBethanecholColforsinDinoprostoneMuscarinic AgonistsSerotoninTrinitrobenzenesulfonic AcidVeratridine

Identifiers

PMID16931576
PMCPMC1856777
OpenAlexW2156563701

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.