Evidence map›Paper›PMID 38111650›Full record

ArticleJournal of immunology research2023

The Expression of Semaphorin3E in Vagal Ganglion and Lung Tissue Is Related to Airway Hyperresponsiveness in Murine Asthma Model.

Liyan Chen, Xiaohui Yuan, Yaowei He, Zichuan Fan, Ya Guan, Qiuying Li, Yaying Chen, Lianglan Bao, Yidan Huang, Kefang Lai

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of immunology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 39% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Review
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

10 authors at 2 institutions in 1 country.

Liyan ChenThe First Affiliated Hospital of Guangzhou Medical University, National Center of Respiratory Medicine, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou 510120, Guangdong, China.ORCID https://orcid.org/0000-0003-2327-439X
Xiaohui YuanThe First Affiliated Hospital of Guangzhou Medical University, National Center of Respiratory Medicine, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou 510120, Guangdong, China.ORCID https://orcid.org/0000-0002-7372-6166
Yaowei HeThe First Affiliated Hospital of Guangzhou Medical University, National Center of Respiratory Medicine, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou 510120, Guangdong, China.
Zichuan FanThe First Affiliated Hospital of Guangzhou Medical University, National Center of Respiratory Medicine, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou 510120, Guangdong, China.
Ya GuanThe First Affiliated Hospital of Guangzhou Medical University, National Center of Respiratory Medicine, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou 510120, Guangdong, China.ORCID https://orcid.org/0009-0003-6540-6247
Qiuying LiThe First Affiliated Hospital of Guangzhou Medical University, National Center of Respiratory Medicine, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou 510120, Guangdong, China.
Yaying ChenThe First Affiliated Hospital of Guangzhou Medical University, National Center of Respiratory Medicine, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou 510120, Guangdong, China.
Lianglan BaoThe First Affiliated Hospital of Guangzhou Medical University, National Center of Respiratory Medicine, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou 510120, Guangdong, China.
Yidan HuangThe First Affiliated Hospital of Guangzhou Medical University, National Center of Respiratory Medicine, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou 510120, Guangdong, China.
Kefang LaiThe First Affiliated Hospital of Guangzhou Medical University, National Center of Respiratory Medicine, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Health, Guangzhou 510120, Guangdong, China.
First Affiliated Hospital of Guangzhou Medical University · CNGuangdong Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Semaphorin3E (Sema3E) mediates reorganization of the actin cytoskeleton, and plays an important role in ensuring the specificity of synapse formation and angiogenesis. However, the role of Sema3E in allergic asthma (AS) and eosinophilic bronchitis (EB) is still elusive. This study aimed to investigate the relationship between Sema3E in vagal ganglion and lung tissue, airway reactivity, and eosinophilic inflammation. Methods: The frequency of coughs and airway reactivity as well as the airway inflammation were observed in ovalbumin- (OVA-) induced AS and EB mouse models. The expression of Sema3E was examined in the vagal ganglion and lung tissues by immunofluorescence staining and western blotting analyses. In the Sema3E treatment protocol, exogenous Sema3E was administrated intranasally before challenge in AS model to study the effect of Sema3E on airway hyperresponsiveness, airway inflammation, mucus production, and collagen deposition. Results: The similar higher frequency of coughs and airway eosinophilic inflammation could be seen in AS and EB groups compared with nasal saline (NS) and dexamethasone (DXM) groups. The absence of the airway hyperresponsiveness was observed in EB and DXM group, while AS group showed increase in airway reactivity to methacholine. The expression of Sema3E in vagal ganglion and lung tissue was remarkably decreased in AS and DXM group compared with EB group. Sema3E-treated asthma mice displayed ameliorated airway hyperresponsiveness, mucus production, and collagen deposition. Conclusion: Sema3E in lungs and vagal ganglia is related to eosinophilic inflammation and has a protective effect on OVA-induced AHR in asthma.

Indexed as

AsthmaEosinophiliaRespiratory HypersensitivityAnimalsBronchoalveolar Lavage FluidCollagenCoughDisease Models, AnimalInflammationLungMiceMice, Inbred BALB COvalbuminCollagenOvalbumin

Identifiers

PMID38111650
PMCPMC10727799
OpenAlexW4389547732

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.