Evidence map›Paper›PMID 19109489›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Nociceptors are interleukin-1beta sensors.

Alexander M Binshtok, Haibin Wang, Katharina Zimmermann, Fumimasa Amaya, Daniel Vardeh, Lin Shi, Gary J Brenner, Ru-Rong Ji, Bruce P Bean, Clifford J Woolf and 1 more

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07109817 (Desloratadine to Prevent Taxane-induced Peripheral Neuropathy in Patients With Breast Cancer), which is not on this map. Cited by 386 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
386citing papers in PubMed, 2 pooled it
11.4field-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.

NCT07109817 phase2recruitingnot on this mapstarted 2026, after this paper: background citation

Desloratadine to Prevent Taxane-induced Peripheral Neuropathy in Patients With Breast Cancer (DETOXp)

TypeinterventionalSponsorMontefiore Medical CenterRan2026 to 2030Enrolled116ConditionsBreast Cancer, Peripheral NeuropathyArmsDesloratodine, Placebo
3 · Its place in the literature

Who cites it

386 citing papers in PubMed, 2 syntheses or guidelines pooled it, 647 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Review
  6. Glial cells in neuropathic pain.Physiological reviews · 2026
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Nociceptor neurons shape antiviral immunity.Journal of neuroinflammation · 2026
    Review
  16. Article
  17. Review
  18. Neuroimmune interactions in cardiovascular homeostasis and disease.American journal of physiology. Cell physiology · 2026
    Review
  19. Review
  20. Article

326 more citing papers are in PubMed but not listed here.

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

11 authors at 4 institutions in 1 country.

Alexander M BinshtokNeural Plasticity Research Group, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Haibin Wang
Katharina Zimmermann
Fumimasa Amaya
Daniel Vardeh
Lin Shi
Gary J Brenner
Ru-Rong Ji
Bruce P Bean
Clifford J Woolf
Tarek A Samad
Massachusetts General Hospital · USHarvard University · USBrigham and Women's Hospital · USPrinceton University · US

Funding

Neural Plasticity and Inflammatory PainR01NS039518 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI WOOLF, CLIFFORD J · 2001 to 2010
$4.1M
NINDS NIH HHS R01 NS039518
6 · The paper itself

Abstract

A cardinal feature of inflammation is heightened pain sensitivity at the site of the inflamed tissue. This results from the local release by immune and injured cells of nociceptor sensitizers, including prostaglandin E(2), bradykinin, and nerve growth factor, that reduce the threshold and increase the excitability of the peripheral terminals of nociceptors so that they now respond to innocuous stimuli: the phenomenon of peripheral sensitization. We show here that the proinflammatory cytokine interleukin-1beta (IL-1beta), in addition to producing inflammation and inducing synthesis of several nociceptor sensitizers, also rapidly and directly activates nociceptors to generate action potentials and induce pain hypersensitivity. IL-1beta acts in a p38 mitogen-activated protein kinase (p38 MAP kinase)-dependent manner, to increase the excitability of nociceptors by relieving resting slow inactivation of tetrodotoxin-resistant voltage-gated sodium channels and also enhances persistent TTX-resistant current near threshold. By acting as an IL-1beta sensor, nociceptors can directly signal the presence of ongoing tissue inflammation.

Indexed as

Action PotentialsAnimalsBiophysicsCells, CulturedDose-Response Relationship, DrugEnzyme InhibitorsGanglia, SpinalImidazolesInterleukin-1betaIntermediate Filament ProteinsMaleMembrane GlycoproteinsNerve Fibers, UnmyelinatedNerve Tissue ProteinsNociceptorsp38 Mitogen-Activated Protein KinasesEnzyme InhibitorsImidazolesInterleukin-1betaIntermediate Filament ProteinsMembrane GlycoproteinsNerve Tissue Proteinsp38 Mitogen-Activated Protein KinasesPeripherinsPyridinesSB 203580Sodium Channel BlockersTetrodotoxin

Identifiers

PMID19109489
PMCPMC2690713
OpenAlexW2157282220

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.