Evidence map›Paper›PMID 23426662›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

The pro-inflammatory cytokines IL-1β and TNFα are neurotrophic for enteric neurons.

P-Y Gougeon, Sandra Lourenssen, Tian Y Han, Dileep G Nair, Mark J Ropeleski, Michael G Blennerhassett

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
10.2field-weighted citation impact, top 1% 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

50 citing papers in PubMed, 96 citations in OpenAlex.

  1. Phenotypic switching of gastrointestinal smooth muscle cells and the regulatory role of macrophages: a literature review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  8. Altered Esophageal Smooth Muscle Phenotype in Achalasia.Journal of neurogastroenterology and motility · 2024
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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

6 authors at 1 institution in 1 country.

P-Y GougeonGastrointestinal Diseases Research Unit, Department of Medicine, Queen's University, Kingston, Ontario K7L 3N6, Canada.
Sandra Lourenssen
Tian Y Han
Dileep G Nair
Mark J Ropeleski
Michael G Blennerhassett
Queen's University · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Intestinal inflammation causes initial axonal degeneration and neuronal death but subsequent axon outgrowth from surviving neurons restores innervation density to the target smooth muscle cells. Elsewhere, the pro-inflammatory cytokines TNFα and IL-1β cause neurotoxicity, leading us to test their role in promoting enteric neuron death. In a rat coculture model, TNFα or IL-1β did not affect neuron number but did promote significant neurite outgrowth to twofold that of control by 48 h, while other cytokines (e.g., IL-4, TGFβ) were without effect. TNFα or IL-1β activated the NFκB signaling pathway, and inhibition of NFκB signaling blocked the stimulation of neurite growth. However, nuclear translocation of NFκB in smooth muscle cells but not in adjacent neurons suggested a dominant role for smooth muscle cells. TNFα or IL-1β sharply increased both mRNA and protein for GDNF, while the neurotrophic effects of TNFα or IL-1β were blocked by the RET-receptor blocker vandetanib. Conditioned medium from cytokine-treated smooth muscle cells mimicked the neurotrophic effect, inferring that TNFα and IL-1β promote neurite growth through NFκB-dependent induction of glial cell line-derived neurotrophic factor (GDNF) expression in intestinal smooth muscle cells. In vivo, TNBS-colitis caused early nuclear translocation of NFκB in smooth muscle cells. Conditioned medium from the intact smooth muscle of the inflamed colon caused a 2.5-fold increase in neurite number in cocultures, while Western blotting showed a substantial increase in GDNF protein. Pro-inflammatory cytokines promote neurite growth through upregulation of GDNF, a novel process that may facilitate re-innervation of smooth muscle cells and a return to homeostasis following initial damage.

Indexed as

AnimalsAnimals, NewbornCells, CulturedCoculture TechniquesEnteric Nervous SystemFemaleGlial Cell Line-Derived Neurotrophic FactorInflammation MediatorsInterleukin-1betaMaleMuscle, SmoothNerve Growth FactorsNeuronsRatsRats, Sprague-DawleyTumor Necrosis Factor-alphaGlial Cell Line-Derived Neurotrophic FactorInflammation MediatorsInterleukin-1betaNerve Growth FactorsTumor Necrosis Factor-alpha

Identifiers

PMID23426662
PMCPMC6619526
OpenAlexW2060215176

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.