Evidence map›Paper›PMID 32047493›Full record

ReviewFrontiers in immunology2019

Neuraxial Cytokines in Pain States.

Gilson Gonçalves Dos Santos, Lauriane Delay, Tony L Yaksh, Maripat Corr

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 2 pooled it
13.0field-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

89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 158 citations in OpenAlex.

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29 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

4 authors at 1 institution in 1 country.

Gilson Gonçalves Dos SantosDepartment of Anesthesiology, University of California, San Diego, La Jolla, CA, United States.
Lauriane DelayDepartment of Anesthesiology, University of California, San Diego, La Jolla, CA, United States.
Tony L YakshDepartment of Anesthesiology, University of California, San Diego, La Jolla, CA, United States.
Maripat CorrDivision of Rheumatology, Allergy and Immunology, University of California, San Diego, La Jolla, CA, United States.
University of California, San Diego · US

Funding

AIBP and regulation of neuropathic painR01NS102432 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MILLER, YURY, YAKSH, TONY L. · 2017 to 2021
$3.0M
Sex, Stress and Immunity in the Acute to Chronic Pain TransitionR01NS099338 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI YAKSH, TONY L. · 2017 to 2021
$1.8M
NINDS NIH HHS R01 NS099338NINDS NIH HHS R01 NS102432
6 · The paper itself

Abstract

A high-intensity potentially tissue-injuring stimulus generates a homotopic response to escape the stimulus and is associated with an affective phenotype considered to represent pain. In the face of tissue or nerve injury, the afferent encoding systems display robust changes in the input-output function, leading to an ongoing sensation reported as painful and sensitization of the nociceptors such that an enhanced pain state is reported for a given somatic or visceral stimulus. Our understanding of the mechanisms underlying this non-linear processing of nociceptive stimuli has led to our appreciation of the role played by the functional interactions of neural and immune signaling systems in pain phenotypes. In pathological states, neural systems interact with the immune system through the actions of a variety of soluble mediators, including cytokines. Cytokines are recognized as important mediators of inflammatory and neuropathic pain, supporting system sensitization and the development of a persistent pathologic pain. Cytokines can induce a facilitation of nociceptive processing at all levels of the neuraxis including supraspinal centers where nociceptive input evokes an affective component of the pain state. We review here several key proinflammatory and anti-inflammatory cytokines/chemokines and explore their underlying actions at four levels of neuronal organization: (1) peripheral nociceptor termini; (2) dorsal root ganglia; (3) spinal cord; and (4) supraspinal areas. Thus, current thinking suggests that cytokines by this action throughout the neuraxis play key roles in the induction of pain and the maintenance of the facilitated states of pain behavior generated by tissue injury/inflammation and nerve injury.

Indexed as

Disease SusceptibilityAnimalsBiomarkersCytokinesGanglia, SpinalGene Expression RegulationGenetic Predisposition to DiseaseHumansMolecular Targeted TherapyMultigene FamilyNociceptorsPainSignal TransductionSpinal CordBiomarkersCytokineschemokinecytokineneuraxisneuroimmune crosstalkpain

Identifiers

PMID32047493
PMCPMC6997465
OpenAlexW3003491238

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.