Evidence map›Paper›PMID 35775903›Full record

ArticleThe Journal of physiology2022

Sensitization of colonic nociceptors by TNFα is dependent on TNFR1 expression and p38 MAPK activity.

Katie H Barker, James P Higham, Luke A Pattison, Toni S Taylor, Iain P Chessell, Fraser Welsh, Ewan St J Smith, David C Bulmer

Open access · hybridAbstract read
In one paragraph

Article in The Journal of physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  7. Review
  8. Article
  9. Coptisine ameliorates colitis in mice by modulating cPLA2/TRPM8/CGRP-1 signaling pathways and strengthening intestinal barrier function.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
    Article
  10. Sensitization of colonic nociceptors by IL-13 is dependent on JAK and p38 MAPK activity.American journal of physiology. Gastrointestinal and liver physiology · 2023
    Article
  11. Review
  12. Article
  13. Article
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

8 authors at 2 institutions in 2 countries.

Katie H BarkerDepartment of Pharmacology, University of Cambridge, Cambridge, UK.ORCID 0000-0002-8601-4416
James P HighamDepartment of Pharmacology, University of Cambridge, Cambridge, UK.
Luke A PattisonDepartment of Pharmacology, University of Cambridge, Cambridge, UK.
Toni S TaylorDepartment of Pharmacology, University of Cambridge, Cambridge, UK.
Iain P ChessellNeuroscience, BioPharmaceuticals R&D, AstraZeneca, Cambridge, UK.
Fraser WelshNeuroscience, BioPharmaceuticals R&D, AstraZeneca, Cambridge, UK.
Ewan St J SmithDepartment of Pharmacology, University of Cambridge, Cambridge, UK.
David C BulmerDepartment of Pharmacology, University of Cambridge, Cambridge, UK.ORCID 0000-0002-4703-7877
University of Cambridge · GBAstraZeneca (United Kingdom) · GB

Funding

Biotechnology and Biological Sciences Research Council BB/M011194/1
6 · The paper itself

Abstract

Visceral pain is a leading cause of morbidity in gastrointestinal diseases, which is exacerbated by the gut-related side-effects of many analgesics. New treatments are needed and further understanding of the mediators and mechanisms underpinning visceral nociception in disease states is required to facilitate this. The pro-inflammatory cytokine TNFα is linked to pain in both patients with inflammatory bowel disease and irritable bowel syndrome, and has been shown to sensitize colonic sensory neurons. Somatic, TNFα-triggered thermal and mechanical hypersensitivity is mediated by TRPV1 signalling and p38 MAPK activity respectively, downstream of TNFR1 receptor activation. We therefore hypothesized that TNFR1-evoked p38 MAPK activity may also be responsible for TNFα sensitization of colonic afferent responses to the TRPV1 agonist capsaicin, and noxious distension of the bowel. Using Ca

Indexed as

NociceptorsVisceral PainAnimalsCapsaicinGanglia, SpinalMicep38 Mitogen-Activated Protein KinasesReceptors, Tumor Necrosis Factor, Type ITRPV Cation ChannelsTumor Necrosis Factor-alphaCapsaicinp38 Mitogen-Activated Protein KinasesReceptors, Tumor Necrosis Factor, Type ITnfrsf1a protein, mouseTRPV Cation ChannelsTumor Necrosis Factor-alphacapsaicininflammatory bowel diseaseirritable bowel syndromenociceptionp38 MAPKTRPV1tumour necrosis factor-alphavisceral pain

Identifiers

PMID35775903
PMCPMC9543404
OpenAlexW4283744444

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.