Evidence map›Paper›PMID 29284473›Full record

ArticleRespiratory research2017

Involvements of p38 MAPK and oxidative stress in the ozone-induced enhancement of AHR and pulmonary inflammation in an allergic asthma model.

Aihua Bao, Hong Yang, Jie Ji, Yuqin Chen, Wuping Bao, Feng Li, Min Zhang, Xin Zhou, Qiang Li, Suqin Ben

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

29 citing papers in PubMed, 51 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

10 authors at 3 institutions in 2 countries.

Aihua BaoDepartment of Respiratory Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, 100 Haining Road, Shanghai, 200080, People's Republic of China.
Hong YangDepartment of Respiratory Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, 100 Haining Road, Shanghai, 200080, People's Republic of China.
Jie JiUnit for Lung and Airway Research, Institute of Environmental Medicine, Karolinska Institutet, PO Box 210, -17177, Stockholm, SE, Sweden.
Yuqin ChenDepartment of Respiratory Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, 100 Haining Road, Shanghai, 200080, People's Republic of China.
Wuping BaoDepartment of Respiratory Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, 100 Haining Road, Shanghai, 200080, People's Republic of China.
Feng LiDepartment of Respiratory Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, 100 Haining Road, Shanghai, 200080, People's Republic of China.
Min ZhangDepartment of Respiratory Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, 100 Haining Road, Shanghai, 200080, People's Republic of China.
Xin ZhouDepartment of Respiratory Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, 100 Haining Road, Shanghai, 200080, People's Republic of China.
Qiang LiDepartment of Respiratory Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, 100 Haining Road, Shanghai, 200080, People's Republic of China.
Suqin BenDepartment of Respiratory Medicine, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, 100 Haining Road, Shanghai, 200080, People's Republic of China. bensuqin@126.com.
Shanghai Jiao Tong University · CNShanghai First People's Hospital · CNKarolinska Institutet · SE

Funding

National Nature Science Foundation of China 81470218National Nature Science Foundation of China 81570018Shanghai Jiao Tong University School of Medicine grant 13XJI0063Shanghai Municipal Commission of Health and Family Planning grant 201440296
6 · The paper itself

Abstract

backgroundExposure to ambient ozone (O

methodsAn ovalbumin (OVA)-established asthmatic mouse model was selected to expose to filtered air (OVA-model) or 1.0 ppm O

resultsIn OVA-allergic mice, O3 exposure deteriorated airway hyperresponsiveness (AHR), airway resistance (Raw), lung compliance (CL) and pulmonary inflammation, accompanied by the increased oxidative stress in lung tissues and promoted p38 MAPK and HSP27 phosphorylation in tracheal tissues. Administration of SB239063 (a p38 MAPK inhibitor) on OVA-O3 model exclusively mitigated the Raw, the CL, and the BAL IL-13 content, while α-tocopherol (antioxidant) differentially reduced the BAL number of eosinophils and macrophages, the content of BAL hyaluronan, the peribronchial inflammation, as well as the mRNA expression of TNF-α and IL-5 in the lung tissues of OVA-O3 model. Administration of these two chemical inhibitors similarly inhibited the AHR, the BAL IFN-γ and IL-6 production, the perivascular lung inflammation and the lung IL-17 mRNA expression of OVA-O3 model. Interestingly, the combined treatment of both compounds together synergistically inhibited neutrophil counts in the BALF and CXCL-1 gene expression in the lung.

conclusionsO

Indexed as

AnimalsAsthmaEnzyme InhibitorsFemaleMiceMice, Inbred BALB COvalbuminOxidative StressOzonep38 Mitogen-Activated Protein KinasesPneumoniaRespiratory HypersensitivityEnzyme InhibitorsOvalbuminOzonep38 Mitogen-Activated Protein KinasesAsthma exacerbationOxidative stressOzonep38 MAPKα-tocopherol

Identifiers

PMID29284473
PMCPMC5747109
OpenAlexW2779191797

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.