ArticleJournal of immunology (Baltimore, Md. : 1950)2016
TLR2 Activation Limits Rhinovirus-Stimulated CXCL-10 by Attenuating IRAK-1-Dependent IL-33 Receptor Signaling in Human Bronchial Epithelial Cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. 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, 38 citations in OpenAlex.
- Bronchial mucosal IFN-α/β and pattern recognition receptor expression in patients with experimental rhinovirus-induced asthma exacerbations.The Journal of allergy and clinical immunology · 2019Trial
- Alarmins differentially modulate airway contraction and relaxation of human small airways.Respiratory research · 2026Review
- The IL-33-ILC2 axis: a key regulator of type 2 immunity in respiratory disease.Frontiers in immunology · 2026Review
- Quercetin improves epithelial regeneration from airway basal cells of COPD patients.Respiratory research · 2024Article
- IRAK-M Regulates Proliferative and Invasive Phenotypes of Lung Fibroblasts.Inflammation · 2023Article
- IL-33/ST2 signaling promotes constitutive and inductive PD-L1 expression and immune escape in oral squamous cell carcinoma.British journal of cancer · 2023Article
- Vimentin affects inflammation and neutrophil recruitment in airway epithelium during Streptococcus suis serotype 2 infection.Veterinary research · 2023Article
- Involvement of Il-33 in the Pathogenesis and Prognosis of Major Respiratory Viral Infections: Future Perspectives for Personalized Therapy.Biomedicines · 2022Review
- Priming With Rhinovirus Protects Mice Against a Lethal Pulmonary Coronavirus Infection.Frontiers in immunology · 2022Article
- Article
- Calcitriol attenuates TLR2/IL-33 signaling pathway to repress Th9 cell differentiation and potentially limits the pathophysiology of rheumatoid arthritis.Molecular and cellular biochemistry · 2021Article
- Viral Induced Effects on a Vulnerable Epithelium; Lessons Learned From Paediatric Asthma and Eosinophilic Oesophagitis.Frontiers in immunology · 2021Review
- Review
- Microarray analysis identifies defects in regenerative and immune response pathways in COPD airway basal cells.ERJ open research · 2020Article
- Contributions of IL-33 in Non-hematopoietic Lung Cells to Obstructive Lung Disease.Frontiers in immunology · 2020Review
- Rhinovirus and Innate Immune Function of Airway Epithelium.Frontiers in cellular and infection microbiology · 2020Review
- Rhinovirus-Induced SIRT-1 via TLR2 Regulates Subsequent Type I and Type III IFN Responses in Airway Epithelial Cells.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Interleukin 1 Receptor-Like 1 (IL1RL1) Promotes Airway Bacterial and Viral Infection and Inflammation.Infection and immunity · 2019Article
- Transcriptomic Analysis Reveals Priming of The Host Antiviral Interferon Signaling Pathway by BronchobiniInternational journal of molecular sciences · 2019Article
- Rhinovirus-induces progression of lung disease in a mouse model of COPD via IL-33/ST2 signaling axis.Clinical science (London, England : 1979) · 2019Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Airway epithelial cells are the major target for rhinovirus (RV) infection and express proinflammatory chemokines and antiviral cytokines that play a role in innate immunity. Previously, we demonstrated that RV interaction with TLR2 causes ILR-associated kinase-1 (IRAK-1) depletion in both airway epithelial cells and macrophages. Further, IRAK-1 degradation caused by TLR2 activation was shown to inhibit ssRNA-induced IFN expression in dendritic cells. Therefore, in this study, we examined the role of TLR2 and IRAK-1 in RV-induced IFN-β, IFN-λ1, and CXCL-10, which require signaling by viral RNA. In airway epithelial cells, blocking TLR2 enhanced RV-induced expression of IFNs and CXCL-10. By contrast, IRAK-1 inhibition abrogated RV-induced expression of CXCL-10, but not IFNs in these cells. Neutralization of IL-33 or its receptor, ST2, which requires IRAK-1 for signaling, inhibited RV-stimulated CXCL-10 expression. In addition, RV induced expression of both ST2 and IL-33 in airway epithelial cells. In macrophages, however, RV-stimulated CXCL-10 expression was primarily dependent on TLR2/IL-1R. Interestingly, in a mouse model of RV infection, blocking ST2 not only attenuated RV-induced CXCL-10, but also lung inflammation. Finally, influenza- and respiratory syncytial virus-induced CXCL-10 was also found to be partially dependent on IL-33/ST2/IRAK-1 signaling in airway epithelial cells. Together, our results indicate that RV stimulates CXCL-10 expression via the IL-33/ST2 signaling axis, and that TLR2 signaling limits RV-induced CXCL-10 via IRAK-1 depletion at least in airway epithelial cells. To our knowledge, this is the first report to demonstrate the role of respiratory virus-induced IL-33 in the induction of CXCL-10 in airway epithelial cells.
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