Evidence map›Paper›PMID 33717165›Full record

ReviewFrontiers in immunology2021

Ozone-Induced Oxidative Stress, Neutrophilic Airway Inflammation, and Glucocorticoid Resistance in Asthma.

Chioma Enweasor, Cameron H Flayer, Angela Haczku

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 3 pooled it
4.8field-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

38 citing papers in PubMed, 3 syntheses or guidelines pooled it, 76 citations in OpenAlex.

  1. A molecular systems architecture of asthma.Frontiers in immunology · 2026
    Pooled it
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  12. Asthma endotypes and theratypes.Chinese medical journal pulmonary and critical care medicine · 2026
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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

3 authors at 2 institutions in 1 country.

Chioma EnweasorUC Davis Lung Center, University of California, Davis, CA, United States.
Cameron H FlayerCenter for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States.
Angela HaczkuUC Davis Lung Center, University of California, Davis, CA, United States.
University of California, Davis · USMassachusetts General Hospital · US

Funding

UC Davis Environmental Health Sciences Core CenterP30ES023513 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Irva Hertz-Picciotto · 2015 to 2026
$26.0M
TRAINING IN COMPARATIVE LUNG BIOLOGY AND MEDICINET32HL007013 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI Elena Goncharova, Nicholas J. KENYON · 1985 to 2026
$10.1M
Research Training in Pulmonary Immunology and Allergy at MGHT32HL116275 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI David C Christiani, ANDREW D LUSTER · 2013 to 2026
$8.6M
ENVIRONMENTAL TOXICOLOGYT32ES007059 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura S Van Winkle · 1985 to 2026
$7.9M
IND enabling development of LGM2605 as adjuvant treatment for asthmaR42AI132012 · NIAID · LIGNAMED, LLC · PI HACZKU, ANGELA, SIELECKI, THAIS MOTRIA · 2019 to 2021
$3.0M
Asthma, anxiety and GR abnormalities in non-human primatesR21AI116121 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HACZKU, ANGELA · 2015 to 2016
$448k
Effects of LGM2605 on a Primate Model of AsthmaR41AI132012 · NIAID · LIGNAMED, LLC · PI HACZKU, ANGELA, SIELECKI, THAIS MOTRIA · 2017 to 2017
$278k
NHLBI NIH HHS T32 HL007013NHLBI NIH HHS T32 HL116275NIAID NIH HHS R21 AI116121NIAID NIH HHS R41 AI132012NIAID NIH HHS R42 AI132012NIEHS NIH HHS P30 ES023513NIEHS NIH HHS T32 ES007059
6 · The paper itself

Abstract

Despite recent advances in using biologicals that target Th2 pathways, glucocorticoids form the mainstay of asthma treatment. Asthma morbidity and mortality remain high due to the wide variability of treatment responsiveness and complex clinical phenotypes driven by distinct underlying mechanisms. Emerging evidence suggests that inhalation of the toxic air pollutant, ozone, worsens asthma by impairing glucocorticoid responsiveness. This review discusses the role of oxidative stress in glucocorticoid resistance in asthma. The underlying mechanisms point to a central role of oxidative stress pathways. The primary data source for this review consisted of peer-reviewed publications on the impact of ozone on airway inflammation and glucocorticoid responsiveness indexed in PubMed. Our main search strategy focused on cross-referencing "asthma and glucocorticoid resistance" against "ozone, oxidative stress, alarmins, innate lymphoid, NK and γδ T cells, dendritic cells and alveolar type II epithelial cells, glucocorticoid receptor and transcription factors". Recent work was placed in the context from articles in the last 10 years and older seminal research papers and comprehensive reviews. We excluded papers that did not focus on respiratory injury in the setting of oxidative stress. The pathways discussed here have however wide clinical implications to pathologies associated with inflammation and oxidative stress and in which glucocorticoid treatment is essential.

Indexed as

AnimalsAsthmaDrug ResistanceGlucocorticoidsHumansInflammationMiceNeutrophilsOxidative StressOzoneRespiratory SystemGlucocorticoidsOzoneair pollutionasthmaglucocorticoid resistanceIL-17Aneutrophilsoxidative stressozone

Identifiers

PMID33717165
PMCPMC7952990
OpenAlexW3135046236

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.