ArticleAllergy2020
IL-1β prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early-life rhinovirus infection in mice.
Article in Allergy, 2020. 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, 33 citations in OpenAlex.
- Breaking the bottleneck of asthma treatment: the future of omni-targeted therapy.Journal of advanced research · 2026Review
- The context-dependent role of group 2 innate lymphoid cells in lung diseases.Acta biochimica et biophysica Sinica · 2026Review
- Article
- Pyroptosis in Respiratory Virus Infections: A Narrative Review of Mechanisms, Pathophysiology, and Potential Therapeutic Interventions.Microorganisms · 2025Review
- In Vivo Model to Assess the Nasal Infection by Minor Group Rhinovirus.Methods in molecular biology (Clifton, N.J.) · 2025Article
- NLRP3 regulates epithelial barrier integrity and protects from airway hyperresponsiveness in experimental allergic asthma.Frontiers in immunology · 2025Article
- Infection of Immature Mice with Rhinovirus for the Study of Asthma Pathogenesis.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Toll-like receptor activation induces airway obstruction and hyperresponsiveness in guinea pigs.Respiratory research · 2024Article
- Tissue-specific features of innate lymphoid cells in antiviral defense.Cellular & molecular immunology · 2024Review
- Early-life pulmonary viral infection leads to long-term functional and lower airway structural changes in the lungs.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Immunotherapeutic implications on targeting the cytokines produced in rhinovirus-induced immunoreactions.Frontiers in allergy · 2024Review
- Review
- NLRP3 inhibition improves maternal hypertension, inflammation, and vascular dysfunction in response to placental ischemia.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
- Tissue-resident immunity in the lung: a first-line defense at the environmental interface.Seminars in immunopathology · 2022Review
- ILC2s in Virus-induced Asthma Exacerbations: A Starring or Supportive Role?American journal of respiratory and critical care medicine · 2021Article
- Deficient inflammasome activation permits an exaggerated asthma phenotype in rhinovirus C-infected immature mice.Mucosal immunology · 2021Article
- Indoleamine 2,3-Dioxygenase in Hematopoietic Stem Cell-Derived Cells Suppresses Rhinovirus-Induced Neutrophilic Airway Inflammation by Regulating Th1- and Th17-Type Responses.Immune network · 2021Article
- A crosstalk between type 2 innate lymphoid cells and alternative macrophages in lung development and lung diseases (Review).Molecular medicine reports · 2021Review
- The Role of Innate Lymphoid Cells in Chronic Respiratory Diseases.Frontiers in immunology · 2021Review
- Abnormal Airway Mucus Secretion Induced by Virus Infection.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEarly-life wheezing-associated respiratory infection with human rhinovirus (RV) is associated with asthma development. RV infection of 6-day-old immature mice causes mucous metaplasia and airway hyperresponsiveness which is associated with the expansion of IL-13-producing type 2 innate lymphoid cells (ILC2s) and dependent on IL-25 and IL-33. We examined regulation of this asthma-like phenotype by IL-1β.
methodsSix-day-old wild-type or NRLP3-/- mice were inoculated with sham or RV-A1B. Selected mice were treated with IL-1 receptor antagonist (IL-1RA), anti-IL-1β, or recombinant IL-1β.
resultsRhinovirus infection induced Il25, Il33, Il4, Il5, Il13, muc5ac, and gob5 mRNA expression, ILC2 expansion, mucus metaplasia, and airway hyperresponsiveness. RV also induced lung mRNA and protein expression of pro-IL-1β and NLRP3 as well as cleavage of caspase-1 and pro-IL-1β, indicating inflammasome priming and activation. Lung macrophages were a major source of IL-1β. Inhibition of IL-1β signaling with IL-1RA, anti-IL-1β, or NLRP3 KO increased RV-induced type 2 cytokine immune responses, ILC2 number, and mucus metaplasia, while decreasing IL-17 mRNA expression. Treatment with IL-1β had the opposite effect, decreasing IL-25, IL-33, and mucous metaplasia while increasing IL-17 expression. IL-1β and IL-17 each suppressed Il25, Il33, and muc5ac mRNA expression in cultured airway epithelial cells. Finally, RV-infected 6-day-old mice showed reduced IL-1β mRNA and protein expression compared to mature mice.
conclusionMacrophage IL-1β limits type 2 inflammation and mucous metaplasia following RV infection by suppressing epithelial cell innate cytokine expression. Reduced IL-1β production in immature animals provides a mechanism permitting asthma development after early-life viral infection.
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