ArticleJournal of translational medicine2015
Rhinoviral stimuli, epithelial factors and ATP signalling contribute to bronchial smooth muscle production of IL-33.
Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Unmasking programmed cell death in rhinovirus-driven asthma pathology.Biochemical Society transactions · 2026Review
- Article
- Potential of IL-33 as a Novel Myokine in Sarcopenia- Osteoporosis Communication: Insights from Mendelian Randomization.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Dexamethasone Suppresses IL-33-exacerbated Malignant Phenotype of U87MG Glioblastoma CellsAnti-cancer agents in medicinal chemistry · 2024Article
- P2XAmerican journal of physiology. Lung cellular and molecular physiology · 2023Article
- Rhinovirus induces airway remodeling: what are the physiological consequences?Respiratory research · 2023Review
- Hepatic pannexin-1 mediates ST2Clinical and translational medicine · 2022Article
- Involvement of Il-33 in the Pathogenesis and Prognosis of Major Respiratory Viral Infections: Future Perspectives for Personalized Therapy.Biomedicines · 2022Review
- Targeting the P2YAmerican journal of respiratory and critical care medicine · 2022Article
- Epithelial miR-206 targets CD39/extracellular ATP to upregulate airway IL-25 and TSLP in type 2-high asthma.JCI insight · 2021Article
- Rhinovirus and Cell Death.Viruses · 2021Review
- Influenza A virus enhances ciliary activity and mucociliary clearance via TLR3 in airway epithelium.Respiratory research · 2020Article
- TLR3/TAK1 signalling regulates rhinovirus-induced interleukin-33 in bronchial smooth muscle cells.ERJ open research · 2020Article
- Contributions of IL-33 in Non-hematopoietic Lung Cells to Obstructive Lung Disease.Frontiers in immunology · 2020Review
- Oxidative stress enhances the expression of IL-33 in human airway epithelial cells.Respiratory research · 2018Article
- Neonatal Immunity, Respiratory Virus Infections, and the Development of Asthma.Frontiers in immunology · 2018Review
- Purinergic Signalling: Therapeutic Developments.Frontiers in pharmacology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBronchial smooth muscle cells (BSMCs) from severe asthmatics have been shown to overexpress the Th2-driving and asthma-associated cytokine IL-33. However, little is known regarding factors involved in BSMC production of IL-33. Rhinovirus (RV) infections cause asthma exacerbations, which exhibit features of Th2-type inflammation. Here, we investigated the effects of epithelial-derived media and viral stimuli on IL-33 expression in human BSMCs.
methodsPrimary human BSMCs from healthy (n = 3) and asthmatic (n = 3) subjects were stimulated with conditioned media from primary human bronchial epithelial cells (BECs), double-stranded (ds)RNA, dsRNA/LyoVec, or infected with RV. BSMCs were also pretreated with the purinergic receptor antagonist suramin. IL-33 expression was analysed by RT-qPCR and western blot and ATP levels were determined in cell supernatants.
resultsRV infection and activation of TLR3 by dsRNA increased IL-33 mRNA and protein in healthy and asthmatic BSMCs. These effects were inhibited by dexamethasone. BSMC expression of IL-33 was also increased by stimulation of RIG-I-like receptors using dsRNA/LyoVec. Conditioned media from BECs induced BSMC expression of IL-33, which was further enhanced by dsRNA. BEC-derived medium and viral-stimulated BSMC supernatants exhibited elevated ATP levels. Blocking of purinergic signalling with suramin inhibited BSMC expression of IL-33 induced by dsRNA and BEC-derived medium.
conclusionsRV infection of BSMCs and activation of TLR3 and RIG-I-like receptors cause expression and production of IL-33. Epithelial-released factor(s) increase BSMC expression of IL-33 and exhibit positive interaction with dsRNA. Increased BSMC IL-33 associates with ATP release and is antagonised by suramin. We suggest that epithelial-derived factors contribute to baseline BSMC IL-33 production, which is further augmented by RV infection of BSMCs and stimulation of their pathogen-recognising receptors.
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