Evidence map›Paper›PMID 27437787›Full record

ArticlePain2016

Mouse model of imiquimod-induced psoriatic itch.

Kent Sakai, Kristen M Sanders, Marina R Youssef, Kevin M Yanushefski, Liselotte Jensen, Gil Yosipovitch, Tasuku Akiyama

Open access · greenAbstract read
In one paragraph

Article in Pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
6.1field-weighted citation impact, top 4% 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

56 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
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  7. Maladaptive immunity to the microbiota promotes neuronal hyperinnervation and itch via IL-17A.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  11. Inactivation of cofilin-1 in Mcpt5-Cre-nf-Cfl1Frontiers in immunology · 2025
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  12. Review
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  17. Multi-target mechanism ofSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
    Article
  18. Article
  19. 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.

Kent SakaiDepartment of Dermatology, Temple Itch Center, Temple University, Philadelphia, PA, USA.
Kristen M SandersDepartment of Dermatology, Temple Itch Center, Temple University, Philadelphia, PA, USA.
Marina R YoussefDepartment of Dermatology, Temple Itch Center, Temple University, Philadelphia, PA, USA.
Kevin M YanushefskiDepartment of Dermatology, Temple Itch Center, Temple University, Philadelphia, PA, USA.
Liselotte JensenDepartment of Microbiology and Immunology, Temple Autoimmunity Center, Temple University, Philadelphia, PA, USA.
Gil YosipovitchDepartment of Dermatology, Temple Itch Center, Temple University, Philadelphia, PA, USA.
Tasuku AkiyamaDepartment of Dermatology, Temple Itch Center, Temple University, Philadelphia, PA, USA.
Temple University · US

Funding

Warmth enhancement of itch via TRPV4R00AR063228 · NIAMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI AKIYAMA, TASUKU · 2014 to 2016
$705k
Warmth enhancement of itch via TRPV4K99AR063228 · NIAMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI AKIYAMA, TASUKU · 2013 to 2014
$176k
NIAMS NIH HHS K99 AR063228NIAMS NIH HHS R00 AR063228
6 · The paper itself

Abstract

Itch is a major indicator of psoriasis, but the underlying mechanisms behind this symptom are largely unknown. To investigate the neuronal mechanisms of psoriatic itch, we tested whether mice subjected to the imiquimod-induced psoriasis model exhibit itch-associated behaviors. Mice received daily topical applications of imiquimod to the rostral back skin for 7 days. Imiquimod-treated mice exhibited a significant increase in spontaneous scratching behavior directed to the treated area as well as touch-evoked scratching (alloknesis). To characterize this model, we measured the mRNA expression levels of pruritogens and itch-relevant receptors/channels using real-time reverse transcription PCR. The mRNA expression of MrgprA3, MrgprC11, and MrgprD decreased gradually over time in the dorsal root ganglion (DRG) cells. There was no significant change in the mRNA expression of TRPV1 or TRPA1 in DRG cells. TRPV4 mRNA expression was transiently increased in the DRG cells, whereas TRPM8 mRNA was significantly decreased. The mRNA expression levels of histidine decarboxylase and tryptophan hydroxylase 1, as well as the intensity of histamine and serotonin immunoreactivity, were transiently increased in the skin on day 2, returning to baseline by day 7. Histamine H1-receptor antagonists, chlorpheniramine and olopatadine, significantly inhibited spontaneous scratching on day 2, but not day 7. Neither chlorpheniramine nor olopatadine affected alloknesis on day 2 or day 7. These results may reflect the limited antipruritic effects of histamine H1-receptor antagonists on human psoriasis. The imiquimod-induced psoriasis model seems to be useful for the investigation of itch and its sensitization in psoriasis.

Indexed as

Disease Models, AnimalAdjuvants, ImmunologicAminoquinolinesAnimalsAnti-Inflammatory Agents, Non-SteroidalAntipruriticsChlorpheniramineGanglia, SpinalGene Expression RegulationHistidine DecarboxylaseImiquimodMaleMiceMice, Inbred C57BLOlopatadine HydrochloridePain MeasurementAdjuvants, ImmunologicAminoquinolinesAnti-Inflammatory Agents, Non-SteroidalAntipruriticsChlorpheniramineHistidine DecarboxylaseImiquimodOlopatadine HydrochlorideTph1 protein, mouseTRPV1 protein, mouseTRPV Cation ChannelsTryptophan Hydroxylase

Identifiers

PMID27437787
PMCPMC5069152
OpenAlexW2497709384

What OpenQuestion holds

Textmetadata
LicenceTDM
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.