ArticlePloS one2013
IL-18 induces airway hyperresponsiveness and pulmonary inflammation via CD4+ T cell and IL-13.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Biomarkers of rheumatoid arthritis-associated interstitial lung disease: a systematic review and meta-analysis.Frontiers in immunology · 2024Pooled it
- Review
- NLRP3 inflammasome in health and disease (Review).International journal of molecular medicine · 2025Review
- Allergens induce upregulated IL-18 and IL-18Rα expression in blood Th2 and Th17 cells of patients with allergic asthma.Clinical and experimental immunology · 2024Article
- Soluble form of the MDA5 protein in human sera.Heliyon · 2024Article
- Unraveling the role of NLRP3 inflammasome in allergic inflammation: implications for novel therapies.Frontiers in immunology · 2024Review
- Pyroptosis in asthma: inflammatory phenotypes, immune and non-immune cells, and novel treatment approaches.Frontiers in pharmacology · 2024Review
- IL-18 biology in severe asthma.Frontiers in medicine · 2024Review
- Inflammasome signalling pathway in the regulation of inflammation - its involvement in the development and exacerbation of asthma and chronic obstructive pulmonary disease.Postepy dermatologii i alergologii · 2023Review
- Inflammatory Biomarkers in the Diagnosis and Prognosis of Rheumatoid Arthritis-Associated Interstitial Lung Disease.International journal of molecular sciences · 2023Observational
- Interleukin-18 Binding Protein in Immune Regulation and Autoimmune Diseases.Biomedicines · 2022Review
- Role of IL-18-transformed CD274-expressing eosinophils in promoting airway obstruction in experimental asthma.Allergy · 2022Article
- The expression analysis of IL-6, IL-18, IL-21, IL-23, and TGF-β mRNA in the nasal mucosa of patients with Allergic rhinitis.African health sciences · 2022Article
- Engineered Small Extracellular Vesicles as a FGL1/PD-L1 Dual-Targeting Delivery System for Alleviating Immune Rejection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Protective role of scutellarin on LPS induced - Acute lung injury and regulation of apoptosis, oxidative stress and reduction of mitochondrial dysfunction.Saudi journal of biological sciences · 2022Article
- Adenovirus vector-mediated YKL-40 shRNA attenuates eosinophil airway inflammation in a murine asthmatic model.Gene therapy · 2021Article
- NLRP3 played a role in Trichinella spiralis-triggered Th2 and regulatory T cells response.Veterinary research · 2020Article
- The Role of T Cells and Macrophages in Asthma Pathogenesis: A New Perspective on Mutual Crosstalk.Mediators of inflammation · 2020Article
- Synergy of Interleukin (IL)-5 and IL-18 in eosinophil mediated pathogenesis of allergic diseases.Cytokine & growth factor reviews · 2019Review
- Interleukin-18: Biological properties and role in disease pathogenesis.Immunological reviews · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IL-18 plays a key role in the pathogenesis of pulmonary inflammatory diseases including pulmonary infection, pulmonary fibrosis, lung injury and chronic obstructive pulmonary disease (COPD). However, it is unknown whether IL-18 plays any role in the pathogenesis of asthma. We hypothesized that overexpression of mature IL-18 protein in the lungs may exacerbate disease activities of asthma. We established lung-specific IL-18 transgenic mice on a Balb/c genetic background. Female mice sensitized- and challenged- with antigen (ovalbumin) were used as a mouse asthma model. Pulmonary inflammation and emphysema were not observed in the lungs of naïve transgenic mice. However, airway hyperresponsiveness and airway inflammatory cells accompanied with CD4(+) T cells, CD8(+) T cells, eosinophils, neutrophils, and macrophages were significantly increased in ovalbumin-sensitized and challenged transgenic mice, as compared to wild type Balb/c mice. We also demonstrate that IL-18 induces IFN-γ, IL-13, and eotaxin in the lungs of ovalbumin-sensitized and challenged transgenic mice along with an increase in IL-13 producing CD4(+) T cells. Treatment with anti-CD4 monoclonal antibody or deletion of the IL-13 gene improves ovalbumin-induced airway hyperresponsiveness and reduces airway inflammatory cells in transgenic mice. Overexpressing the IL-18 protein in the lungs induces type 1 and type 2 cytokines and airway inflammation, and results in increasing airway hyperresponsiveness via CD4(+) T cells and IL-13 in asthma.
Indexed as
Identifiers
What OpenQuestion holds
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.