Evidence map›Paper›PMID 31608051›Full record

ReviewFrontiers in immunology2019

Acute Respiratory Barrier Disruption by Ozone Exposure in Mice.

Milena Sokolowska, Valerie F J Quesniaux, Cezmi A Akdis, Kian Fan Chung, Bernhard Ryffel, Dieudonnée Togbe

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Oxeiptosis - potential in cancer treatment?Expert reviews in molecular medicine · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
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  19. Review
  20. Inhaled ozone induces distinct alterations in pulmonary function in models of acute and episodic exposure in female mice.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    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

6 authors at 4 institutions in 3 countries.

Milena SokolowskaSwiss Institute of Allergy and Asthma Research, University of Zurich, Davos, Switzerland.
Valerie F J QuesniauxLaboratory of Experimental and Molecular Immunology and Neurogenetics (INEM), UMR 7355 CNRS-University of Orleans, Orléans, France.
Cezmi A AkdisSwiss Institute of Allergy and Asthma Research, University of Zurich, Davos, Switzerland.
Kian Fan ChungAirways Disease, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Bernhard RyffelLaboratory of Experimental and Molecular Immunology and Neurogenetics (INEM), UMR 7355 CNRS-University of Orleans, Orléans, France.
Dieudonnée TogbeLaboratory of Experimental and Molecular Immunology and Neurogenetics (INEM), UMR 7355 CNRS-University of Orleans, Orléans, France.
Centre National de la Recherche Scientifique · FRUniversity of Zurich · CHImperial College London · GBUniversité d'Orléans · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ozone exposure causes irritation, airway hyperreactivity (AHR), inflammation of the airways, and destruction of alveoli (emphysema), the gas exchange area of the lung in human and mice. This review focuses on the acute disruption of the respiratory epithelial barrier in mice. A single high dose ozone exposure (1 ppm for 1 h) causes first a break of the bronchiolar epithelium within 2 h with leak of serum proteins in the broncho-alveolar space, disruption of epithelial tight junctions and cell death, which is followed at 6 h by ROS activation, AHR, myeloid cell recruitment, and remodeling. High ROS levels activate a novel PGAM5 phosphatase dependent cell-death pathway, called oxeiptosis. Bronchiolar cell wall damage and inflammation upon a single ozone exposure are reversible. However, chronic ozone exposure leads to progressive and irreversible loss of alveolar epithelial cells and alveoli with reduced gas exchange space known as emphysema. It is further associated with chronic inflammation and fibrosis of the lung, resembling other environmental pollutants and cigarette smoke in pathogenesis of asthma, and chronic obstructive pulmonary disease (COPD). Here, we review recent data on the mechanisms of ozone induced injury on the different cell types and pathways with a focus on the role of the IL-1 family cytokines and the related IL-33. The relation of chronic ozone exposure induced lung disease with asthma and COPD and the fact that ozone exacerbates asthma and COPD is emphasized.

Indexed as

Acute DiseaseAnimalsAsthmaBlood-Air BarrierCigarette SmokingHumansMiceOzonePhosphoprotein PhosphatasesPneumoniaPulmonary Disease, Chronic ObstructivePulmonary EmphysemaReactive Oxygen SpeciesRespiratory MucosaTight JunctionsOzonePGAM5 protein, mousePhosphoprotein PhosphatasesReactive Oxygen Speciescell deathinflammationinnate immunityinterleukinsmucustight junctions

Identifiers

PMID31608051
PMCPMC6758598
OpenAlexW2970433500

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.