Evidence map›Paper›PMID 30509328›Full record

ArticleJournal of neuroinflammation2018

Regulatory role of capsaicin-sensitive peptidergic sensory nerves in the proteoglycan-induced autoimmune arthritis model of the mouse.

Ádám Horváth, Éva Borbély, Kata Bölcskei, Nikolett Szentes, Tamás Kiss, Mátyás Belák, Tibor Rauch, Tibor Glant, Róza Zákány, Tamás Juhász and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Ameliorated Autoimmune Arthritis and Impaired B Cell Receptor-Mediated CaInternational journal of molecular sciences · 2020
    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

14 authors at 3 institutions in 2 countries.

Ádám HorváthDepartment of Pharmacology and Pharmacotherapy, University of Pécs Medical School, Szigeti u. 12, Pécs, 7624, Hungary.
Éva BorbélyDepartment of Pharmacology and Pharmacotherapy, University of Pécs Medical School, Szigeti u. 12, Pécs, 7624, Hungary.
Kata BölcskeiDepartment of Pharmacology and Pharmacotherapy, University of Pécs Medical School, Szigeti u. 12, Pécs, 7624, Hungary.
Nikolett SzentesDepartment of Pharmacology and Pharmacotherapy, University of Pécs Medical School, Szigeti u. 12, Pécs, 7624, Hungary.
Tamás KissDepartment of Pharmacology and Pharmacotherapy, University of Pécs Medical School, Szigeti u. 12, Pécs, 7624, Hungary.
Mátyás BelákDepartment of Pharmacology and Pharmacotherapy, University of Pécs Medical School, Szigeti u. 12, Pécs, 7624, Hungary.
Tibor RauchDepartment of Orthopedic Surgery, Section of Molecular Medicine, Rush University Medical Center, Chicago, USA.
Tibor GlantDepartment of Orthopedic Surgery, Section of Molecular Medicine, Rush University Medical Center, Chicago, USA.
Róza ZákányDepartment of Anatomy, Histology, and Embryology, University of Debrecen, Debrecen, Hungary.
Tamás JuhászDepartment of Anatomy, Histology, and Embryology, University of Debrecen, Debrecen, Hungary.
Edina KaranyiczDepartment of Anatomy, Histology, and Embryology, University of Debrecen, Debrecen, Hungary.
Ferenc BoldizsárMedical School, Department of Immunology, University of Pécs, Pécs, Hungary.
Zsuzsanna HelyesDepartment of Pharmacology and Pharmacotherapy, University of Pécs Medical School, Szigeti u. 12, Pécs, 7624, Hungary. zsuzsanna.helyes@aok.pte.hu.
Bálint BotzJános Szentágothai Research Centre, Molecular Pharmacology Research Team and Centre for Neuroscience, University of Pécs, Pécs, Hungary.
University of Pecs · HUUniversity of Debrecen · HURush University Medical Center · US

Funding

Mapping of Arthritis Susceptibility GenesR01AR059356 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI GLANT, TIBOR T. · 2010 to 2014
$2.2M
A Gene Regulatory Network Controlled by Transcription Factor ZBTB38 in RAR21AR064948 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI RAUCH, TIBOR ATTILA · 2013 to 2014
$348k
EFOP, Hungary EFOP-3.6.2-16-2017-00008GINOP, Hungary GINOP-2.3.2-15-2016-00050Hungarian Academy of Sciences Bolyai János ScholarshipHungarian Academy of Sciences Magyary Zoltán FundHungarian Academy of Sciences Szodoray Lajos FundNational Brain Research Program, Hungary 20017-1.2.1-NKP-2017-00002New National Excellence Program of the Ministry of Human Capacities, Hungary ÚNKP-17-3-III-PTE-79New National Excellence Program of the Ministry of Human Capacities, Hungary ÚNKP-17-4-I-PTE-96NIAMS NIH HHS R01 AR059356NIAMS NIH HHS R21 AR064948NIH HHS R01 AR059356NIH HHS R21 AR064948
6 · The paper itself

Abstract

objectiveThe regulatory role of capsaicin-sensitive peptidergic sensory nerves has been shown in acute inflammation, but little is known about their involvement in T/B-cell driven autoimmune arthritis. This study integratively characterized the function of these nerve endings in the proteoglycan-induced chronic arthritis (PGIA), a translational model of rheumatoid arthritis.

methodsPeptidergic afferents were defunctionalized by resiniferatoxin (RTX) pretreatment in BALB/c mice, PGIA was induced by repeated antigen challenges. Hind paw volume, arthritis severity, grasping ability and the mechanonociceptive threshold were monitored during the 17-week experiment. Myeloperoxidase activity, vascular leakage and bone turnover were evaluated by in vivo optical imaging. Bone morphology was assessed using micro-CT, the intertarsal small joints were processed for histopathological analysis.

resultsFollowing desensitization of the capsaicin-sensitive afferents, ankle edema, arthritis severity and mechanical hyperalgesia were markedly diminished. Myeloperoxidase activity was lower in the early, but increased in the late phase, whilst plasma leakage and bone turnover were not altered. Desensitized mice displayed similar bone spurs and erosions, but increased trabecular thickness of the tibia and bony ankylosis of the spine. Intertarsal cartilage thickness was not altered in the model, but desensitization increased this parameter in both the non-arthritic and arthritic groups.

conclusionThis is the first integrative in vivo functional and morphological characterization of the PGIA mouse model, wherein peptidergic afferents have an important regulatory function. Their overall effect is proinflammatory by increasing acute inflammation, immune cell activity and pain. Meanwhile, their activation decreases spinal ankylosis, arthritis-induced altered trabecularity, and cartilage thickness in small joints.

Indexed as

AnimalsAnkleArthritis, RheumatoidCapsaicinCartilageDisease Models, AnimalDiterpenesFemaleHindlimbMiceMice, Inbred BALB CNeurotoxinsPeptidesProteoglycansReactive Oxygen SpeciesSensory System AgentsCapsaicinDiterpenesNeurotoxinsPeptidesProteoglycansReactive Oxygen SpeciesresiniferatoxinSensory System AgentsExperimental arthritisMouse modelNeurogenic inflammationNociceptionRheumatoid arthritis

Identifiers

PMID30509328
PMCPMC6276168
OpenAlexW2902177212

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.