Evidence map›Paper›PMID 31616413›Full record

ArticleFrontiers in immunology2019

Pharmacological Blockade of Spinal CXCL3/CXCR2 Signaling by NVP CXCR2 20, a Selective CXCR2 Antagonist, Reduces Neuropathic Pain Following Peripheral Nerve Injury.

Anna Piotrowska, Ewelina Rojewska, Katarzyna Pawlik, Grzegorz Kreiner, Agata Ciechanowska, Wioletta Makuch, Irena Nalepa, Joanna Mika

Open access · goldAbstract read
In one paragraph

Article 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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  6. Chemokines and Their Association With Symptom Severity in Women With Endometriosis.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025
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  16. CC Chemokine Receptor 4 (CCR4) as a Possible New Target for Therapy.International journal of molecular sciences · 2022
    Review
  17. Review
  18. 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

8 authors at 2 institutions in 1 country.

Anna PiotrowskaDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
Ewelina RojewskaDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
Katarzyna PawlikDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
Grzegorz KreinerDepartment of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
Agata CiechanowskaDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
Wioletta MakuchDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
Irena NalepaDepartment of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
Joanna MikaDepartment of Pain Pharmacology, Maj Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
Maj Institute of Pharmacology · PLPolish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, the role of CXCR2 in nociception has been noted. Our studies provide new evidence that the intrathecal administration of its CINC ligands (Cytokine-Induced Neutrophil Chemoattractant; CXCL1-3) induces pain-like behavior in naïve mice, and the effect occurring shortly after administration is associated with the neural location of CXCR2, as confirmed by immunofluorescence. RT-qPCR analysis showed, for the first time, raised levels of spinal CXCR2 after chronic constriction injury (CCI) of the sciatic nerve in rats. Originally, on day 2, we detected escalated levels of the spinal mRNA of all CINCs associated with enhancement of the protein level of CXCL3 lasting until day 7. Intrathecal administration of CXCL3 neutralizing antibody diminished neuropathic pain on day 7 after CCI. Interestingly, CXCL3 is produced in lipopolysaccharide-stimulated microglial, but not astroglial, primary cell cultures. We present the first evidence that chronic intrathecal administrations of the selective CXCR2 antagonist, NVP CXCR2 20, attenuate neuropathic pain symptoms and CXCL3 expression after CCI. Moreover, in naïve mice, this antagonist prevented CXCL3-induced hypersensitivity. However, NVP CXCR2 20 did not diminish glial activation, thus not enhancing morphine/buprenorphine analgesia. These results provide novel insight into the crucial role of CXCR2 in neuropathy based on CXCL3 modulation, which may become a potential therapeutic target in pain treatment.

Indexed as

AnimalsChemokines, CXCMaleMiceMicrogliaNeuralgiaPeripheral Nerve InjuriesRatsRats, WistarReceptors, Interleukin-8BSciatic NerveSignal TransductionSpinal CordChemokines, CXCCxcl3 protein, ratCxcr2 protein, ratReceptors, Interleukin-8BastrogliaCXCL1CXCL2gliamicroglia

Identifiers

PMID31616413
PMCPMC6775284
OpenAlexW2971130976

What OpenQuestion holds

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LicenceCC BY
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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.