Evidence map›Paper›PMID 30982974›Full record

ArticleAllergy2019

Benzo(a)pyrene facilitates dermatophagoides group 1 (Der f 1)-induced epithelial cytokine release through aryl hydrocarbon receptor in asthma.

Eryi Wang, Xiaoyu Liu, Wei Tu, Danh C Do, Haiqiong Yu, Liteng Yang, Yufeng Zhou, Damo Xu, Shau-Ku Huang, Pingchang Yang and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Allergy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.9field-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

37 citing papers in PubMed, 79 citations in OpenAlex.

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  15. The Effects and Pathogenesis of PM2.5 and Its Components on Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023
    Review
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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

13 authors at 5 institutions in 4 countries.

Eryi WangThe Affiliated Luohu Hospital of Shenzhen University, Shenzhen Luohu Hospital Group, Shenzhen, China.
Xiaoyu LiuThe State Key Laboratory of Respiratory Disease for Allergy, Shenzhen University School of Medicine, Shenzhen University, Shenzhen, China.
Wei TuThe Affiliated Luohu Hospital of Shenzhen University, Shenzhen Luohu Hospital Group, Shenzhen, China.
Danh C DoJohns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Haiqiong YuThe Affiliated Luohu Hospital of Shenzhen University, Shenzhen Luohu Hospital Group, Shenzhen, China.
Liteng YangThe Affiliated Luohu Hospital of Shenzhen University, Shenzhen Luohu Hospital Group, Shenzhen, China.
Yufeng ZhouKey Laboratory of Neonatal Disease, Ministry of Health, Children's Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Damo XuInstitute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK.
Shau-Ku HuangThe Affiliated Luohu Hospital of Shenzhen University, Shenzhen Luohu Hospital Group, Shenzhen, China.
Pingchang YangThe Affiliated Luohu Hospital of Shenzhen University, Shenzhen Luohu Hospital Group, Shenzhen, China.
Pixin RanGuangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Pei-Song GaoJohns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0000-0002-7651-1339
Zhigang LiuThe Affiliated Luohu Hospital of Shenzhen University, Shenzhen Luohu Hospital Group, Shenzhen, China.
Shenzhen University · CNJohns Hopkins University · USChildren's Hospital of Fudan University · CNState Key Laboratory of Respiratory Disease · CNUniversity of Glasgow · GB

Funding

Sensitization to Cockroach Allergen: Immune Regulation and Genetic DeterminantsR01ES021739 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2013 to 2017
$1.8M
Mannose Receptor, miR-511-3p, and Macrophage Polarization in AsthmaR21AI121768 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2016 to 2017
$462k
Regulation of allergen-induced mast cell activation and allergic inflammation through DCIRR21AI137547 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2018 to 2019
$450k
Lineage Commitment of Mesenchymal Stem Cell in Allergen-induced Airway RemodelingR21AI109062 · NIAID · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2014 to 2015
$446k
NIAID NIH HHS R21 AI109062NIAID NIH HHS R21 AI121768NIAID NIH HHS R21 AI137547NIEHS NIH HHS R01 ES021739
6 · The paper itself

Abstract

backgroundEnvironmental pollutants, which coexist with allergens, have been associated with the exacerbation of asthma. However, the underlying molecular mechanisms remain elusive. We sought to determine whether benzo(a)pyrene (BaP) co-exposure with dermatophagoides group 1 allergen (Der f 1) can potentiate Der f 1-induced asthma and its underlying mechanisms.

methodsThe effect of BaP was investigated in Der f 1-induced mouse model of asthma, including airway hyper-responsiveness, allergic inflammation, and epithelial-derived cytokines. The impact of BaP on Der f 1-induced airway epithelial cell oxidative stress (ROS) and cytokine release was further analyzed. The role of aryl hydrocarbon receptor (AhR) signaling in BaP-promoted Der f 1-induced ROS, cytokine production, and allergic inflammation was also investigated.

resultsCompared with Der f 1, BaP co-exposure with Der f 1 led to airway hyper-responsiveness and increased lung inflammation in mouse model of asthma. Increased expression of TSLP, IL-33, and IL-25 was also found in the airways of these mice. Moreover, BaP co-exposure with Der f 1 activated AhR signaling with increased expression of AhR and CYP1A1 and promoted airway epithelial ROS generation and TSLP and IL-33, but not IL-25, expression. Interestingly, AhR antagonist CH223191 or cells with AhR knockdown abrogated the increased expression of ROS, TSLP, and IL-33. Furthermore, ROS inhibitor N-acetyl-L-cysteine (NAC) also suppressed BaP co-exposure-induced expression of epithelial TSLP, IL-33, and IL-25. Finally, AhR antagonist CH223191 and NAC inhibited BaP co-exposure with Der f 1-induced lung inflammation.

conclusionsOur findings suggest that BaP facilitates Der f 1-induced epithelial cytokine release through the AhR-ROS axis.

Indexed as

AllergensAnimalsAntigens, DermatophagoidesArthropod ProteinsAsthmaBenzo(a)pyreneCysteine EndopeptidasesCytokinesDisease Models, AnimalEnvironmental PollutantsEpithelial CellsHumansMiceReactive Oxygen SpeciesReceptors, Aryl HydrocarbonRespiratory MucosaAllergensAntigens, DermatophagoidesArthropod ProteinsBenzo(a)pyreneCysteine EndopeptidasesCytokinesDermatophagoides farinae antigen f 1Environmental PollutantsReactive Oxygen SpeciesReceptors, Aryl HydrocarbonAryl hydrocarbon receptorbenzo(a)pyrene (BaP)dermatophagoides group 1 allergen (Der f 1)IL-25IL-33reactive oxygen speciesTSLP

Identifiers

PMID30982974
PMCPMC6790621
OpenAlexW2937615137

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.