Evidence map›Paper›PMID 31093659›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2019

Interleukin 33 Expression Induced by Aryl Hydrocarbon Receptor in Macrophages.

Yasuhiro Ishihara, Thomas Haarmann-Stemmann, Norman Y Kado, Christoph F A Vogel

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Targeting IL-33 in Precision Neuroimmunology: Cellular Mechanisms and Therapeutic Strategies for CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Mechanisms underlying aryl hydrocarbon receptor-driven divergent macrophage function.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Emerging Effects of IL-33 on COVID-19.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
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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

4 authors at 3 institutions in 3 countries.

Yasuhiro IshiharaCenter for Health and the Environment, University of California, Davis 95616, California.
Thomas Haarmann-StemmannLeibniz Research Institute for Environmental Medicine, Düsseldorf 40225, Germany.
Norman Y KadoCenter for Health and the Environment, University of California, Davis 95616, California.
Christoph F A VogelCenter for Health and the Environment, University of California, Davis 95616, California.
University of California, Davis · USHiroshima University · JPLeibniz Institute of Environmental Medicine · DE

Funding

Air pollution, atherosclerosis, and the role of the aryl hydrocarbon receptorR01ES029126 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI VOGEL, CHRISTOPH F A · 2019 to 2023
$1.8M
Importance of AhR for the cellular function and communication of dendritic cellsR01ES019898 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI VOGEL, CHRISTOPH F A · 2012 to 2016
$1.7M
The protective role of the AhR Repressor in breast cancer developmentR21ES030419 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI VOGEL, CHRISTOPH F A · 2019 to 2020
$432k
NIEHS NIH HHS R01 ES019898NIEHS NIH HHS R01 ES029126NIEHS NIH HHS R21 ES030419
6 · The paper itself

Abstract

Polycyclic aromatic hydrocarbons (PAHs) contained in airborne particulate matter have been identified as a contributing factor for inflammation in the respiratory tract. Recently, interleukin-33 (IL-33) is strongly suggested to be associated with airway inflammation. Aryl hydrocarbon receptor (AhR) is a receptor for PAHs to regulate several metabolic enzymes, but the relationships between AhR and airway inflammation are still unclear. In this study, we examined the role of AhR in the expression of IL-33 in macrophages. THP-1 macrophages mainly expressed IL-33 variant 5, which in turn was strongly induced by the AhR agonists 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) and kynurenine (KYN). AhR antagonist CH223191 suppressed the increase in IL-33 expression. Promoter analysis revealed that the IL-33 promoter has 2 dioxin response elements (DREs). AhR was recruited to both DREs after treatment with TCDD or KYN as assessed by gel shift and chromatin immunoprecipitation assays. A luciferase assay showed that one of the DREs was functional and involved in the expression of IL-33. Macrophages isolated from AhR-null mice expressed only low levels of IL-33 even in response to treatment with AhR ligands compared with wild-type cells. The treatment of THP-1 macrophages with diesel particulate matter and particle extracts increased the mRNA and protein expression of IL-33. Taken together, the results show that ligand-activated AhR mediates the induction of IL-33 in macrophages via a DRE located in the IL-33 promoter region. AhR-mediated IL-33 induction could be involved in the exacerbation and/or prolongation of airway inflammation elicited by toxic chemical substances.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsExonsHumansInflammationInterleukin-33KynurenineMacrophagesMaleMiceMice, Inbred C57BLPolychlorinated DibenzodioxinsPromoter Regions, GeneticReceptors, Aryl HydrocarbonResponse ElementsTHP-1 CellsAHR protein, humanBasic Helix-Loop-Helix ProteinsInterleukin-33KynureninePolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonAhRdiesel particulate matterIL-33macrophages

Identifiers

PMID31093659
PMCPMC6657576
OpenAlexW2946665091

What OpenQuestion holds

Textmetadata
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.