ArticleThe Journal of allergy and clinical immunology2016
Group 2 innate lymphoid cells mediate ozone-induced airway inflammation and hyperresponsiveness in mice.
Article in The Journal of allergy and clinical immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Effects of Air Pollution on Lung Innate Lymphoid Cells: Review of In Vitro and In Vivo Experimental Studies.International journal of environmental research and public health · 2019Pooled it
- Impacts of Environmental Pollutants on Innate Immunity: The Role of Group 2 Innate Lymphoid Cells.Clinical reviews in allergy & immunology · 2026Review
- MyD88 mediates allergic airway inflammation by regulating ILC2s function through inducing the formation of P38/GATA3 complex.Respiratory research · 2026Article
- Osteopontin from monocyte-derived dendritic cells mediates ozone-induced pulmonary responses in mice.Frontiers in immunology · 2026Article
- Advances in the Gut-Lung Axis and Bronchial Asthma: From Mechanisms to Therapeutic Potential.Clinical and translational allergy · 2025Review
- Group 2 innate lymphoid cells derived IL-9 reduces macrophage apoptosis and attenuates acute lung injury in sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- PIP-seq identifies novel heterogeneous lung innate lymphocyte population activation after combustion product exposure.Scientific reports · 2024Article
- Ozone as an environmental driver of influenza.Nature communications · 2024Article
- Chemical respiratory sensitization-Current status of mechanistic understanding, knowledge gaps and possible identification methods of sensitizers.Frontiers in toxicology · 2024Review
- "Air That Once Was Breath" Part 1: Wildfire-Smoke-Induced Mechanisms of Airway Inflammation - "Climate Change, Allergy and Immunology" Special IAAI Article Collection: Collegium Internationale Allergologicum Update 2023.International archives of allergy and immunology · 2024Review
- Ozone impairs endogenous compensatory responses in allergic asthma.Toxicology and applied pharmacology · 2023Article
- Pla2g2a promotes innate Th2-type immunity lymphocytes to increase B1a cells.Scientific reports · 2022Article
- Emerging Insights into the Impact of Air Pollution on Immune-Mediated Asthma Pathogenesis.Current allergy and asthma reports · 2022Review
- Role of TRPA1/TRPV1 in acute ozone exposure induced murine model of airway inflammation and bronchial hyperresponsiveness.Journal of thoracic disease · 2022Article
- A neutrophil/TGF-β axis limits the pathogenicity of allergen-specific CD4+ T cells.JCI insight · 2022Article
- Article
- Nanoparticle-Induced Airway Eosinophilia Is Independent of ILC2 Signaling but Associated With Sex Differences in Macrophage Phenotype Development.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Memory-like innate lymphoid cells in the pathogenesis of asthma.Frontiers in immunology · 2022Review
- Research Advances in the Treatment of Allergic Rhinitis by Probiotics.Journal of asthma and allergy · 2022Review
- A Novel Nonhuman Primate Model of Nonatopic Asthma.Methods in molecular biology (Clifton, N.J.) · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundAsthmatic patients are highly susceptible to air pollution and in particular to the effects of ozone (O3) inhalation, but the underlying mechanisms remain unclear.
objectiveUsing mouse models of O3-induced airway inflammation and airway hyperresponsiveness (AHR), we sought to investigate the role of the recently discovered group 2 innate lymphoid cells (ILC2s).
methodsC57BL/6 and BALB/c mice were exposed to Aspergillus fumigatus, O3, or both (3 ppm for 2 hours). ILC2s were isolated by means of fluorescence-activated cell sorting and studied for Il5 and Il13 mRNA expression. ILC2s were depleted with anti-Thy1.2 mAb and replaced by means of intratracheal transfer of ex vivo expanded Thy1.1 ILC2s. Cytokine levels (ELISA and quantitative PCR), inflammatory cell profile, and AHR (flexiVent) were assessed in the mice.
resultsIn addition to neutrophil influx, O3 inhalation elicited the appearance of eosinophils and IL-5 in the airways of BALB/c but not C57BL/6 mice. Although O3-induced expression of IL-33, a known activator of ILC2s, in the lung was similar between these strains, isolated pulmonary ILC2s from O3-exposed BALB/c mice had significantly greater Il5 and Il13 mRNA expression than C57BL/6 mice. This suggested that an altered ILC2 function in BALB/c mice might mediate the increased O3 responsiveness. Indeed, anti-Thy1.2 treatment abolished but ILC2s added back dramatically enhanced O3-induced AHR.
conclusionsO3-induced activation of pulmonary ILC2s was necessary and sufficient to mediate asthma-like changes in BALB/c mice. This previously unrecognized role of ILC2s might help explain the heightened susceptibility of human asthmatic airways to O3 exposure.
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Registered trials
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.