ArticleAmerican journal of respiratory cell and molecular biology2013
Interleukin-1 receptor and caspase-1 are required for the Th17 response in nitrogen dioxide-promoted allergic airway disease.
Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 52 citations in OpenAlex.
- Group 3 Innate Lymphoid Cells: A Potential Therapeutic Target for Steroid Resistant Asthma.Clinical reviews in allergy & immunology · 2024Review
- To investigate the function of age-related genes in different subtypes of asthma based on bioinformatics analysis.Heliyon · 2024Article
- Inhibition of phosphoinositide 3-kinase activity attenuates neutrophilic airway inflammation and inhibits pyrin domain-containing 3 inflammasome activation in an ovalbumin-lipopolysaccharide-induced asthma murine model.Molecular biology reports · 2024Article
- Leukotriene BBiomedicines · 2021Article
- Emerging role of air pollution and meteorological parameters in COVID-19.Journal of evidence-based medicine · 2021Review
- Therapeutic efficacy of IL-17A neutralization with corticosteroid treatment in a model of antigen-driven mixed-granulocytic asthma.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- MiR-223 plays a protecting role in neutrophilic asthmatic mice through the inhibition of NLRP3 inflammasome.Respiratory research · 2020Article
- Leptin facilitates the differentiation of Th17 cells from MRL/Mp-Fas lpr lupus mice by activating NLRP3 inflammasome.Innate immunity · 2020Article
- Increased Weekly Mean PMFrontiers in veterinary science · 2020Article
- Targeting NLRP3 Inflammasome Activation in Severe Asthma.Journal of clinical medicine · 2019Review
- Ambient Air Pollution and Daily Hospital Admissions for Respiratory Disease in Children in Guiyang, China.Frontiers in pediatrics · 2019Article
- The Iron Chelator and Anticancer Agent Dp44mT Relieves Allergic Inflammation in Mice With Allergic Rhinitis.Inflammation · 2018Article
- Casticin inhibits interleukin-1β-induced ICAM-1 and MUC5AC expression by blocking NF-κB, PI3K-Akt, and MAPK signaling in human lung epithelial cells.Oncotarget · 2017Article
- Uricase Inhibits Nitrogen Dioxide-Promoted Allergic Sensitization to Inhaled Ovalbumin Independent of Uric Acid Catabolism.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Mechanisms of Asthma in Obesity. Pleiotropic Aspects of Obesity Produce Distinct Asthma Phenotypes.American journal of respiratory cell and molecular biology · 2016Review
- Resistin-Like Molecule α in Allergen-Induced Pulmonary Vascular Remodeling.American journal of respiratory cell and molecular biology · 2015Article
- Immunological characteristics and management considerations in obese patients with asthma.Expert review of clinical immunology · 2015Review
- Inflammasome Activity in Non-Microbial Lung Inflammation.Journal of environmental immunology and toxicology · 2014Article
- Outdoor air pollution and asthma.Lancet (London, England) · 2014Review
- Update in environmental and occupational lung diseases 2013.American journal of respiratory and critical care medicine · 2014Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Nitrogen dioxide (NO2) is an environmental pollutant and endogenously generated oxidant associated with the development, severity, and exacerbation of asthma. NO2 exposure is capable of allergically sensitizing mice to the innocuous inhaled antigen ovalbumin (OVA), promoting neutrophil and eosinophil recruitment, and a mixed Th2/Th17 response upon antigen challenge that is reminiscent of severe asthma. However, the identity of IL-17A-producing cells and the mechanisms governing their ontogeny in NO2-promoted allergic airway disease remain unstudied. We measured the kinetics of lung inflammation after antigen challenge in NO2-promoted allergic airway disease, including inflammatory cells in bronchoalveolar lavage and antigen-specific IL-17A production from the lung. We determined that IL-17A(+) cells were predominately CD4(+)T cell receptor (TCR)β(+) Th17 cells, and that a functional IL-1 receptor was required for Th17, but not Th2, cytokine production after in vitro antigen restimulation of lung cells. The absence of natural killer T cells, γδ T cells, or the inflammasome scaffold nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain (Nlrp)3 did not affect the development of NO2-promoted allergic inflammation or IL-17A production. Similarly, neutrophil depletion or the neutralization of IL-1α during sensitization exerted no effect on these parameters. However, the absence of caspase-1 significantly reduced IL-17A production from lung cells without affecting Th2 cytokines or lung inflammation. Finally, the intranasal administration of IL-1β and the inhalation of antigen promoted allergic sensitization that was reflected by neutrophilic airway inflammation and IL-17A production from CD4(+)TCRβ(+) Th17 cells subsequent to antigen challenge. These data implicate a role for caspase-1 and IL-1β in the IL-1 receptor-dependent Th17 response manifest in NO2-promoted allergic airway disease.
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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.