Evidence map›Paper›PMID 32938460›Full record

ArticleRespiratory research2020

Pentraxin 3 promotes airway inflammation in experimental asthma.

Pengfei Gao, Kun Tang, Yanjiao Lu, Zhenli Huang, Shanshan Wang, Meijia Wang, Jianmiao Wang, Jianping Zhao, Jungang Xie

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 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.

Pengfei GaoDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, National Clinical Research Center of Respiratory Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Kun TangDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, National Clinical Research Center of Respiratory Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Yanjiao LuDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, National Clinical Research Center of Respiratory Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Zhenli HuangDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, National Clinical Research Center of Respiratory Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Shanshan WangDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, National Clinical Research Center of Respiratory Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Meijia WangDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, National Clinical Research Center of Respiratory Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Jianmiao WangDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, National Clinical Research Center of Respiratory Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Jianping ZhaoDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, National Clinical Research Center of Respiratory Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China. jpzhaotj@163.com.
Jungang XieDepartment of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, National Clinical Research Center of Respiratory Disease, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China. xiejjgg@hotmail.com.ORCID http://orcid.org/0000-0001-9037-3027
Tongji Hospital · CNFirst Affiliated Hospital of Henan University of Science and Technology · CN

Funding

National Basic Research Program of China (973 Program) 20l5CB553403National Key R&D Program of China 2016YFC1304500National Key R&D Program of China 2018YFC1311900National Natural Science Foundation of China 81370145National Natural Science Foundation of China 81570033National Natural Science Foundation of China 81973986
6 · The paper itself

Abstract

backgroundPentraxin 3 (PTX3) regulates multiple aspects of innate immunity and tissue inflammation. Recently, it has been reported that PTX3 deficiency enhances interleukin (IL)-17A-dominant pulmonary inflammation in an ovalbumin (OVA)-induced mouse asthma model. However, whether PTX3 treatment would provide protection against allergic airway inflammation has not been clearly elucidated. The goal of this study was to further investigate the effect of recombinant PTX3 administration on the phenotype of asthma.

methodsC57BL/6 J mice were sensitized and challenged with OVA to induce eosinophilic asthma model, as well as sensitized with OVA plus LPS and challenged with OVA to induce neutrophilic asthma model. We evaluated effect of recombinant PTX3 on asthma phenotype through both asthma models. The bronchoalveolar lavage fluid (BALF) inflammatory cells and cytokines, airway hyperresponsiveness, and pathological alterations of the lung tissues were assessed.

resultsIn both eosinophilic and neutrophilic asthma models, PTX3 treatment provoked airway hyperresponsiveness, concomitant with increased inflammatory cytokines IL-4, IL-17, eotaxin, and transforming growth factor (TGF)-β1 and aggravated airway accumulation of inflammatory cells, especially eosinophils and neutrophils. In histological analysis of the lung tissue, administration of PTX3 promoted inflammatory cells infiltration, mucus production, and collagen deposition. In addition, PTX3 also significantly enhanced STAT3 phosphorylation in lung tissue.

conclusionOur results show that exogenous PTX3 can exacerbate multiple asthmatic features by promoting both eosinophils and neutrophils lung infiltration and provide new evidence to better understand the complex role of PTX3 in allergic airway inflammation.

Indexed as

AnimalsAsthmaC-Reactive ProteinFemaleInflammation MediatorsMiceMice, Inbred C57BLNerve Tissue ProteinsOvalbuminPentraxinsC-Reactive ProteinInflammation MediatorsNerve Tissue ProteinsOvalbuminPentraxinsAirway inflammationAsthmaEosinophilNeutrophilPTX3

Identifiers

PMID32938460
PMCPMC7493172
OpenAlexW3085364605

What OpenQuestion holds

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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.