ArticlePloS one2016
IL-25 Promotes Th2 Immunity Responses in Asthmatic Mice via Nuocytes Activation.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- CAR-NKT Cells in Asthma: Use of NKT as a Promising Cell for CAR Therapy.Clinical reviews in allergy & immunology · 2024Review
- Article
- Targeting the Epithelium-Derived Innate Cytokines: From Bench to Bedside.Immune network · 2022Review
- Review
- ML-7 attenuates airway inflammation and remodeling via inhibiting the secretion of Th2 cytokines in mice model of asthma.Molecular medicine reports · 2018Article
- Biological Properties and the Role of IL-25 in Disease Pathogenesis.Journal of immunology research · 2018Review
- Interleukin-25 primed mesenchymal stem cells achieve better therapeutic effects on dextran sulfate sodium-induced colitis via inhibiting Th17 immune response and inducing T regulatory cell phenotype.American journal of translational research · 2017Article
- Reference Values for a Panel of Cytokinergic and Regulatory Lymphocyte Subpopulations.Immune network · 2016Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInterleukin-25 (IL-25) is a potent activator of type-2 immune responses, and is responsible for airway inflammation in asthma. Previous reports have shown that IL-25 expressed hyper-reactivity in an experimental mouse-model of asthma. In addition, the production of IL-13/IL-5 promoted by nuocytes induced airway inflammation. Thus, it has been questioned whether blocking IL-25 against its receptor IL-17BR could inhibit the expression of IL-13 and IL-5 via nuocytes, and further protect against inflammation in ovalbumin (OVA) induced mouse-model of asthma.
methodsIn this study, in order to investigate the correlation among IL-25, IL-5, IL-13 and nuocyte activities, we used OVA-sensitization and -challenging to induce the mouse model of asthma. The murine asthmatic model was validated by histology. The expressions of IL-5, IL-13 and IL-25 were detected by ELISA, quantitative real-time PCR, and western blotting of the lung tissue. Nuocyte activation was identified by the levels of ICOS (clone C398.4A) and T1/ST2 (cloneDJ8) (acting as nuocytes surface markers) in the bronchoalveolar lavage fluid (BALF). This, in turn, was done by means of flow cytometry. The expressions of IL-25, IL-5 and IL-13 in our murine model were detected in the BALF.
resultsThe mice sensitized and challenged with OVA showed a high expression of IL-25 in both the mRNA and protein levels in lungs. The expressions of ICOS and T1/ST2 in BALF were increased. A significant correlation between IL-25 mRNA, protein, and other Th2-cell producing cytokines (such as IL-5 and IL-13) moreover were identified. Furthermore, when the asthmatic mice were treated with anti-IL-25, both the inflammatory cells' infiltration and the inflammatory cytokines' secretion were significantly decreased. The present findings indicate that IL-25 might be involved in a series of asthmatic immune responses, playing an important role in the increase of nuocytes, and that its activation is necessary in maintaining Th2 central memory and sustaining asthmatic inflammation.
conclusionThis study showed that IL-25 promoted the accumulation of ICOS and T1/ST2 on nuocytes, further induced the pro-inflammatory Th2 cells, and promoted Th2 cytokine responses in OVA-induced airway inflammation.
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