Evidence map›Paper›PMID 42229868›Full record

ArticleThe journal of pain2026

A critical role for α7 nicotinic acetylcholine receptor signaling in myeloid lineage cells in chronic neuropathic and inflammatory pain responses.

Alexis Swift, Martial Caillaud, Alexandru Graur, Bryan D McKiver, Wisam Toma, Eda Koseli, Jared Mann, William B Lynch, Jacob A Beierle, Priyanka Thareja and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The journal of pain, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

19 authors.

Alexis SwiftDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA. Electronic address: alexisjswift@gmail.com.
Martial CaillaudNantes Université, Inserm, TENS, The Enteric Nervous System in Gut and Brain Diseases, IMAD, Nantes, France.
Alexandru GraurSchool of Systems Biology, George Mason University, Fairfax, VA, USA.
Bryan D McKiverDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA; Translational Research Initiative for Pain and Neuropathy, Virginia Commonwealth University, Richmond, VA 23298, USA.
Wisam TomaDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA.
Eda KoseliDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA.
Jared MannDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA.
William B LynchLaboratory of Addiction Genetics, Center for Drug Discovery, Department of Pharmaceutical Sciences, Northeastern University, Boston, MA, USA.
Jacob A Beierle
Priyanka TharejaLaboratory of Addiction Genetics, Center for Drug Discovery, Department of Pharmaceutical Sciences, Northeastern University, Boston, MA, USA.
Emily J YaoLaboratory of Addiction Genetics, Center for Drug Discovery, Department of Pharmaceutical Sciences, Northeastern University, Boston, MA, USA.
Jolene J WindleDepartment of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, VA 23298, USA.
Harvens BeauzileDepartment of Pharmaceutical Sciences, Northeastern University, Boston, MA, USA.
Unsong OhDepartment of Neurology, VCU School of Medicine, Richmond, VA 23298, USA.
Ganesh A ThakurDepartment of Pharmaceutical Sciences, Northeastern University, Boston, MA, USA.
Michael D BurtonNeuroimmunology and Behavior Laboratory, Department of Neuroscience, School of Behavioral and Brain Sciences, Center for Advanced Pain Studies, University of Texas at Dallas, 800 W. Campbell Road, Richardson, TX 75080, USA.
Camron D BryantLaboratory of Addiction Genetics, Center for Drug Discovery, Department of Pharmaceutical Sciences, Northeastern University, Boston, MA, USA.
Nadine KabbaniInterdisciplinary Program in Neuroscience, George Mason University, Fairfax, VA, USA; School of Systems Biology, George Mason University, Fairfax, VA, USA.
M Imad DamajDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA; Translational Research Initiative for Pain and Neuropathy, Virginia Commonwealth University, Richmond, VA 23298, USA. Electronic address: m.damaj@vcuhealth.org.

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Renato Martins · 1985 to 2026
$51.0M
VCU Center for Drug Addiction ResearchP30DA033934 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI JOLENE J WINDLE · 2014 to 2026
$13.8M
(PQ9) Mitigation of chemotherapy induced peripheral neuropathyR01CA206028 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI DAMAJ, M. IMAD, GEWIRTZ, DAVID A. · 2016 to 2020
$1.7M
NCI NIH HHS P30 CA016059NCI NIH HHS R01 CA206028NIDA NIH HHS P30 DA033934
6 · The paper itself

Abstract

Neuroinflammation influences the development of chronic pain, an increasingly prevalent condition impacting the lives of many worldwide. Given the challenges of managing chronic pain, it is essential to explore new neuroimmune targets for the development of safe and effective analgesics. α7 nicotinic acetylcholine receptors (α7 nAChR) have been explored for their role in pain and inflammation. It was hypothesized that α7 nAChR expression within myeloid cells mediates an anti-inflammatory response that mitigates pain states. Two mouse strains were engineered, with deletion of the α7 gene (Chrna7) globally and from myeloid lineage cells conditionally. These mice were characterized in chemotherapy-induced peripheral neuropathy (CIPN) using paclitaxel and acute and chronic inflammatory pain models. Spontaneous and evoked pain-related behaviors, gene expression of pro-inflammatory cytokines in peripheral nervous tissue, and other physiological parameters were measured. Additionally, RNA-sequencing and pathway enrichment analysis of spinal cord tissues from mice treated with paclitaxel were performed. Mice deficient for α7 nAChR in myeloid cells showed a marked increase in evoked pain behaviors in CIPN and chronic inflammatory models with a corresponding increase in gene expression of key pro-inflammatory cytokines in the peripheral sensory nervous system. Enrichment analysis identified changes in pathways pertaining to vascular function and enriched pathways associated with extracellular matrix function and angiogenesis in conditional knock-out mice treated with paclitaxel. This study suggests α7 nAChR expression in myeloid cells mediates an endogenous cholinergic anti-inflammatory pathway, which plays a critical role in chronic neuropathic and inflammatory pain and is an important target for developing novel analgesic agents. PERSPECTIVE: This article presents evidence that α7 nicotinic receptors located on myeloid cells are critical for attenuating neuropathic and chronic inflammatory pain. This provides new insight into a cellular target for the treatment of these conditions.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorChronic PainInflammationMyeloid CellsNeuralgiaNeuroinflammatory DiseasesSignal TransductionAnimalsDisease Models, AnimalMaleMiceMice, KnockoutPaclitaxelalpha7 Nicotinic Acetylcholine ReceptorChrna7 protein, mousePaclitaxelAlpha7 nicotinic receptorInflammationMouseNeuropathyPain

Identifiers

PMID42229868
PMCPMC13632657

What OpenQuestion holds

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Registered trials

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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.