Evidence map›Paper›PMID 35203356›Full record

ArticleCells2022

Aryl Hydrocarbon Receptor (AhR) Limits the Inflammatory Responses in Human Lung Adenocarcinoma A549 Cells via Interference with NF-κB Signaling.

Gerardo Vázquez-Gómez, Martina Karasová, Zuzana Tylichová, Markéta Kabátková, Aleš Hampl, Jason Matthews, Jiří Neča, Miroslav Ciganek, Miroslav Machala, Jan Vondráček

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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  15. Protective Effect ofNutrients · 2022
    Article
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 4 institutions in 3 countries.

Gerardo Vázquez-GómezDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, 61265 Brno, Czech Republic.ORCID 0000-0002-4187-5415
Martina KarasováDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, 61265 Brno, Czech Republic.
Zuzana TylichováDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, 61265 Brno, Czech Republic.
Markéta KabátkováDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, 61265 Brno, Czech Republic.
Aleš HamplDepartment of Histology and Embryology, Faculty of Medicine, Masaryk University, 62500 Brno, Czech Republic.
Jason MatthewsDepartment of Nutrition, Institute of Basic Medical Sciences, University of Oslo, 0372 Oslo, Norway.ORCID 0000-0002-9815-8636
Jiří NečaDepartment of Pharmacology and Toxicology, Veterinary Research Institute, 62100 Brno, Czech Republic.
Miroslav CiganekDepartment of Pharmacology and Toxicology, Veterinary Research Institute, 62100 Brno, Czech Republic.
Miroslav MachalaDepartment of Pharmacology and Toxicology, Veterinary Research Institute, 62100 Brno, Czech Republic.
Jan VondráčekDepartment of Cytokinetics, Institute of Biophysics of the Czech Academy of Sciences, 61265 Brno, Czech Republic.ORCID 0000-0003-4071-1969
Czech Academy of Sciences, Institute of Biophysics · CZVeterinary Research Institute · CZMasaryk University · CZUniversity of Oslo · NO

Funding

Consejo Nacional de Ciencia y Tecnología Postdoctoral stay abroad fellowship No. 324651Czech Academy of Sciences PPLZ no. L200042051Czech Academy of Sciences RVO: 68081707Czech Science Foundation 18-00145SMinistry of Agriculture RO0520
6 · The paper itself

Abstract

Apart from its role in the metabolism of carcinogens, the aryl hydrocarbon receptor (AhR) has been suggested to be involved in the control of inflammatory responses within the respiratory tract. However, the mechanisms responsible for this are only partially known. In this study, we used A549 cell line, as a human model of lung alveolar type II (ATII)-like cells, to study the functional role of the AhR in control of inflammatory responses. Using IL-1β as an inflammation inducer, we found that the induction of cyclooxygenase-2 and secretion of prostaglandins, as well as expression and release of pro-inflammatory cytokines, were significantly higher in the AhR-deficient A549 cells. This was linked with an increased nuclear factor-κB (NF-κB) activity, and significantly enhanced phosphorylation of its regulators, IKKα/β, and their target IκBα, in the AhR-deficient A549 cells. In line with this, when we mimicked the exposure to a complex mixture of airborne pollutants, using an organic extract of reference diesel exhaust particle mixture, an exacerbated inflammatory response was observed in the AhR-deficient cells, as compared with wild-type A549 cells. Together, the present results indicate that the AhR may act as a negative regulator of the inflammatory response in the A549 model, via a direct modulation of NF-κB signaling. Its role(s) in the control of inflammation within the lung alveoli exposed to airborne pollutants, especially those which simultaneously activate the AhR, thus deserve further attention.

Indexed as

Environmental PollutantsInflammationNF-kappa BReceptors, Aryl HydrocarbonA549 CellsHumansEnvironmental PollutantsNF-kappa BReceptors, Aryl HydrocarbonAhRalveolar epithelial type II cellscytokinesinflammationNF-κBprostaglandins

Identifiers

PMID35203356
PMCPMC8870046
OpenAlexW4213168715

What OpenQuestion holds

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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.