Evidence map›Paper›PMID 35354939›Full record

ArticleScientific reports2022

Gene knockdown of CCR3 reduces eosinophilic inflammation and the Th2 immune response by inhibiting the PI3K/AKT pathway in allergic rhinitis mice.

Jiasheng Yuan, Yuehui Liu, Juan Yu, Meina Dai, Yu Zhu, Youwei Bao, Haisen Peng, Ke Liu, Xinhua Zhu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

27 citing papers in PubMed, 41 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Jiasheng YuanDepartment of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Yuehui LiuDepartment of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Juan YuDepartment of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Meina DaiDepartment of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Yu ZhuDepartment of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Youwei BaoDepartment of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Haisen PengDepartment of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Ke LiuDepartment of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Xinhua ZhuDepartment of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China. zhuxinhua2003@126.com.
Nanchang University · CNSecond Affiliated Hospital of Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The CCR3 gene plays a critical role in allergic airway inflammation, such as allergic rhinitis (AR), and there is an inflammatory signal link between the nasal cavity and the CCR3 gene in bone marrow. However, the effects of the CCR3 gene in bone marrow cells on AR are not clear. The present study investigated the roles and underlying mechanisms of the bone marrow CCR3 gene in AR mice. Conditional knockout of the bone marrow CCR3 gene (CKO) in mice was generated using the Cre-LoxP recombination system, and offspring genotypes were identified using polymerase chain reaction (PCR). An ovalbumin-induced AR model was established in CKO and wild-type mice to measure eosinophilic inflammation and the Th2 immune response. The following mechanisms were explored using a specific PI3K/AKT pathway inhibitor (Ly294002). We successfully constructed and bred homozygous CKO mice and confirmed a significant increase in CCR3 expression and PI3K/AKT pathway activity in AR mice. Deficiency of the bone marrow CCR3 gene caused a remarkable reduction of CCR3 expression and the PI3K/AKT signaling pathway activity, inhibited histopathological lesions and eosinophil infiltration of the nasal cavity, and reduced the production of Th2 cytokines in serum, which led to the remission of allergic symptoms in AR mice. Ly294002 treatment also decreased these inflammatory indexes in a concentration-dependent manner and blocked inflammatory signals from CCR3, but it did not affect the high expression of CCR3 in AR mice. Collectively, our results suggest that conditional knockout of the bone marrow CCR3 gene can reduce eosinophilic inflammation and the Th2 immune response, which may be due to inhibition of the PI3K/AKT pathway.

Indexed as

Phosphatidylinositol 3-KinasesRhinitis, AllergicAnimalsDisease Models, AnimalGene Knockdown TechniquesImmunityInflammationMiceMice, Inbred BALB CNasal MucosaProto-Oncogene Proteins c-aktReceptors, CCR3Ccr3 protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, CCR3

Identifiers

PMID35354939
PMCPMC8969185
OpenAlexW4220822720

What Socratic 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 Socratic graph.