Evidence map›Paper›PMID 26035830›Full record

Trial reportPloS one2015

Inflammatory and repair pathways induced in human bronchoalveolar lavage cells with ozone inhalation.

Pascale Leroy, Andrea Tham, Hofer Wong, Rachel Tenney, Chun Chen, Rachel Stiner, John R Balmes, Agnès C Paquet, Mehrdad Arjomandi

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 3 pooled it
2.7field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 3 syntheses or guidelines pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Gene Expression Analysis to Assess the Relevance of Rodent Models to Human Lung Injury.American journal of respiratory cell and molecular biology · 2017
    Pooled it
  3. Pooled it
  4. Changes in Metabolites Present in Lung-Lining Fluid Following Exposure of Humans to Ozone.Toxicological sciences : an official journal of the Society of Toxicology · 2018
    Trial
  5. Review
  6. Review
  7. Evaluating the role of alveolar macrophages in tolerance to ozone.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Transcriptional Profiling of the Murine Airway Response to Acute Ozone Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
  14. Review
  15. Review
  16. Article
  17. Newly divided eosinophils limit ozone-induced airway hyperreactivity in nonsensitized guinea pigs.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  18. 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

9 authors at 4 institutions in 2 countries.

Pascale LeroySan Francisco Veterans Affairs Medical Center, San Francisco, California, United States of America.
Andrea ThamSan Francisco Veterans Affairs Medical Center, San Francisco, California, United States of America.
Hofer WongHuman Exposure Laboratory, Division of Occupational and Environmental Medicine, University of California San Francisco, San Francisco, California, United States of America; Division of Pulmonary, Critical Care, Allergy and Immunology, and Sleep Medicine, University of California San Francisco, San Francisco, California, United States of America.
Rachel TenneySan Francisco Veterans Affairs Medical Center, San Francisco, California, United States of America.
Chun ChenLung Biology Center, Department of Medicine; University of California San Francisco, San Francisco, California, United States of America.
Rachel StinerSan Francisco Veterans Affairs Medical Center, San Francisco, California, United States of America.
John R BalmesHuman Exposure Laboratory, Division of Occupational and Environmental Medicine, University of California San Francisco, San Francisco, California, United States of America; Division of Pulmonary, Critical Care, Allergy and Immunology, and Sleep Medicine, University of California San Francisco, San Francisco, California, United States of America; Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, California, United States of America.
Agnès C PaquetCentre National de la Recherche Scientifique, Institut de Pharmacologie Moléculaire et Cellulaire, Valbonne, France.
Mehrdad ArjomandiSan Francisco Veterans Affairs Medical Center, San Francisco, California, United States of America; Human Exposure Laboratory, Division of Occupational and Environmental Medicine, University of California San Francisco, San Francisco, California, United States of America; Division of Pulmonary, Critical Care, Allergy and Immunology, and Sleep Medicine, University of California San Francisco, San Francisco, California, United States of America.
San Francisco VA Medical Center · USUniversity of California System · USInstitut de Pharmacologie Moléculaire et Cellulaire · FRUniversity of California, San Francisco · US

Funding

UCSF CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTEUL1RR024131 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JOHNSTON, S. CLAIBORNE · 2006 to 2011
$111.2M
CTSA: K12 COMPONENTKL2RR024130 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JOHNSTON, S. CLAIBORNE · 2006 to 2011
$19.3M
Osteopontin in Oxidative Injury and Airway Remodeling in AsthmaK23HL083099 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ARJOMANDI, MEHRDAD · 2006 to 2010
$744k
NCRR NIH HHS KL2 RR024130NCRR NIH HHS UL1 RR024131NHLBI NIH HHS K23 HL083099
6 · The paper itself

Abstract

backgroundInhalation of ambient levels of ozone causes airway inflammation and epithelial injury.

methodsTo examine the responses of airway cells to ozone-induced oxidative injury, 19 subjects (7 with asthma) were exposed to clean air (0ppb), medium (100ppb), and high (200ppb) ambient levels of ozone for 4h on three separate occasions in a climate-controlled chamber followed by bronchoscopy with bronchoalveolar lavage (BAL) 24h later. BAL cell mRNA expression was examined using Affymetrix GeneChip Microarray. The role of a differentially expressed gene (DEG) in epithelial injury was evaluated in an in vitro model of injury [16HBE14o- cell line scratch assay].

resultsOzone exposure caused a dose-dependent up-regulation of several biologic pathways involved in inflammation and repair including chemokine and cytokine secretion, activity, and receptor binding; metalloproteinase and endopeptidase activity; adhesion, locomotion, and migration; and cell growth and tumorigenesis regulation. Asthmatic subjects had 1.7- to 3.8-fold higher expression of many DEGs suggestive of increased proinflammatory and matrix degradation and remodeling signals. The most highly up-regulated gene was osteopontin, the protein level of which in BAL fluid increased in a dose-dependent manner after ozone exposure. Asthmatic subjects had a disproportionate increase in non-polymerized osteopontin with increasing exposure to ozone. Treatment with polymeric, but not monomeric, osteopontin enhanced the migration of epithelial cells and wound closure in an α9β1 integrin-dependent manner.

conclusionsExpression profiling of BAL cells after ozone exposure reveals potential regulatory genes and pathways activated by oxidative stress. One DEG, osteopontin, promotes epithelial wound healing in an in vitro model of injury.

Indexed as

AsthmaBronchoalveolar Lavage FluidInflammationOsteopontinOzoneAdultAir ConditioningBronchoscopyCell LineCell MovementCluster AnalysisDose-Response Relationship, DrugEpithelial CellsFemaleGene Expression RegulationHumansOsteopontinOzone

Identifiers

PMID26035830
PMCPMC4452717
OpenAlexW590290905

What OpenQuestion holds

Textmetadata
LicenceCC0
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.