Evidence map›Paper›PMID 10079105›Full record

ArticleThe Journal of clinical investigation1999

Neurotensin is a proinflammatory neuropeptide in colonic inflammation.

I Castagliuolo, C C Wang, L Valenick, A Pasha, S Nikulasson, R E Carraway, C Pothoulakis

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

52 citing papers in PubMed, 132 citations in OpenAlex.

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  11. Absence of neurotensin attenuates intestinal dysbiosis and inflammation by maintaining Mmp7/α-defensin axis in diet-induced obese mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  12. Review
  13. Beneficial Effects of Neurotensin in Murine Model of Hapten-Induced Asthma.International journal of molecular sciences · 2019
    Article
  14. The emerging role of lncRNAs in inflammatory bowel disease.Experimental & molecular medicine · 2018
    Review
  15. Role of G protein-coupled receptors-microRNA interactions in gastrointestinal pathophysiology.American journal of physiology. Gastrointestinal and liver physiology · 2017
    Review
  16. Review
  17. Review
  18. Article
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  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

7 authors at 4 institutions in 1 country.

I CastagliuoloDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. icastagl@bidmc.harvard.edu
C C Wang
L Valenick
A Pasha
S Nikulasson
R E Carraway
C Pothoulakis
Harvard University · USBeth Israel Deaconess Medical Center · USBoston Medical Center · USUniversity of Massachusetts Chan Medical School · US

Funding

SUBSTANCE P AND INTESTINAL INFLAMMATIONR01DK047343 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 1994 to 2014
$4.2M
NEUROTENSIN AND ENTEROHEPATIC BILE ACID REGULATIONR01DK028565 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CARRAWAY, ROBERT E · 1986 to 1999
–
NIDDK NIH HHS DK-28565NIDDK NIH HHS DK-47343NIDDK NIH HHS R01 DK047343
6 · The paper itself

Abstract

The neuropeptide neurotensin mediates several intestinal functions, including chloride secretion, motility, and cellular growth. However, whether this peptide participates in intestinal inflammation is not known. Toxin A, an enterotoxin from Clostridium difficile, mediates pseudomembranous colitis in humans. In animal models, toxin A causes an acute inflammatory response characterized by activation of sensory neurons and intestinal nerves and immune cells of the lamina propria. Here we show that neurotensin and its receptor are elevated in the rat colonic mucosa following toxin A administration. Pretreatment of rats with the neurotensin receptor antagonist SR-48, 692 inhibits toxin A-induced changes in colonic secretion, mucosal permeability, and histologic damage. Exposure of colonic explants to toxin A or neurotensin causes mast cell degranulation, which is inhibited by SR-48,692. Because substance P was previously shown to mediate mast cell activation, we examined whether substance P is involved in neurotensin-induced mast cell degranulation. Our results show that neurotensin-induced mast cell degranulation in colonic explants is inhibited by the substance P (neurokinin-1) receptor antagonist CP-96,345, indicating that colonic mast activation in response to neurotensin involves release of substance P. We conclude that neurotensin plays a key role in the pathogenesis of C. difficile-induced colonic inflammation and mast cell activation.

Indexed as

Bacterial ToxinsAnimalsBiphenyl CompoundsCell DegranulationColitisEnterotoxinsIntestinal SecretionsIn Vitro TechniquesMast CellsNeurokinin-1 Receptor AntagonistsNeurotensinPyrazolesQuinolinesRatsReceptor Cross-TalkReceptors, NeurotensinBacterial ToxinsBiphenyl CompoundsCP 96345EnterotoxinsNeurokinin-1 Receptor AntagonistsNeurotensinneurotensin type 1 receptorPyrazolesQuinolinesReceptors, NeurotensinSR 48692tcdA protein, Clostridium difficile

Identifiers

PMID10079105
PMCPMC408137
OpenAlexW2061594143

What OpenQuestion holds

Texttitle and abstract
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.