Evidence map›Paper›PMID 31919846›Full record

ArticleImmunology2020

The blockade of CC chemokine receptor type 1 influences the level of nociceptive factors and enhances opioid analgesic potency in a rat model of neuropathic pain.

Katarzyna Pawlik, Anna Piotrowska, Klaudia Kwiatkowski, Katarzyna Ciapała, Katarzyna Popiolek-Barczyk, Wioletta Makuch, Joanna Mika

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  14. Neuropathic pain; what we know and what we should do about it.Frontiers in pain research (Lausanne, Switzerland) · 2023
    Review
  15. Article
  16. CC Chemokine Receptor 4 (CCR4) as a Possible New Target for Therapy.International journal of molecular sciences · 2022
    Review
  17. Article
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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

7 authors at 1 institution in 1 country.

Katarzyna PawlikDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.ORCID 0000-0002-8091-4974
Anna PiotrowskaDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.ORCID 0000-0002-2091-2678
Klaudia KwiatkowskiDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.ORCID 0000-0002-0119-5749
Katarzyna CiapałaDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.ORCID 0000-0001-6147-1576
Katarzyna Popiolek-BarczykDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.ORCID 0000-0003-4366-6577
Wioletta MakuchDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.ORCID 0000-0002-1579-3643
Joanna MikaDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.ORCID 0000-0003-1986-7205
Maj Institute of Pharmacology · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A growing body of evidence has indicated that the release of nociceptive factors, such as interleukins and chemokines, by activated immune and glial cells has crucial significance for neuropathic pain generation and maintenance. Moreover, changes in the production of nociceptive immune factors are associated with low opioid efficacy in the treatment of neuropathy. Recently, it has been suggested that CC chemokine receptor type 1 (CCR1) signaling is important for nociception. Our study provides evidence that the development of hypersensitivity in rats following chronic constriction injury (CCI) of the sciatic nerve is associated with significant up-regulation of endogenous CCR1 ligands, namely, CCL2, CCL3, CCL4, CCL6, CCL7 and CCL9 in the spinal cord and CCL2, CCL6, CCL7 and CCL9 in dorsal root ganglia (DRG). We showed that single and repeated intrathecal administration of J113863 (an antagonist of CCR1) attenuated mechanical and thermal hypersensitivity. Moreover, repeated administration of a CCR1 antagonist enhanced the analgesic properties of morphine and buprenorphine after CCI. Simultaneously, repeated administration of J113863 reduced the protein levels of IBA-1 in the spinal cord and MPO and CD4 in the DRG and, as a consequence, the level of pronociceptive factors, such as interleukin-1β (IL-1β), IL-6 and IL-18. The data obtained provide evidence that CCR1 blockade reduces hypersensitivity and increases opioid-induced analgesia through the modulation of neuroimmune interactions.

Indexed as

AnalgesicsAnimalsBuprenorphineCalcium-Binding ProteinsChemokine CCL2Disease Models, AnimalDrug SynergismGanglia, SpinalGene Expression RegulationHyperalgesiaInterleukin-18Interleukin-1betaInterleukin-6MaleMicrofilament ProteinsMorphineAif1 protein, ratAnalgesicsBuprenorphineCalcium-Binding ProteinsCcl2 protein, ratCcr1 protein, ratChemokine CCL2IL1B protein, ratIl6 protein, ratInterleukin-18Interleukin-1betaInterleukin-6Microfilament ProteinsMorphinePeroxidaseProtein IsoformsReceptors, CCR1UCB 35625XanthenesbuprenorphineCCR1interleukinsJ113863morphine

Identifiers

PMID31919846
PMCPMC7078003
OpenAlexW2999343058

What OpenQuestion holds

Textmetadata
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.