Association of airway inflammation and smoking status with IL-33 level in sputum of patients with asthma or COPD
Asthma and COPD are heterogeneous inflammatory airway conditions. Interleukin (IL)-33 is an epithelial pleiotropic cytokine that regulates type 1 and type 2 immune responses [1]. Clinical trials have shown promising efficacy of monoclonal antibodies targeting IL-33 and its ST2 receptor in asthma and...
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| Main Authors: | , , , , , , , |
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| Format: | Article (Journal) Editorial |
| Language: | English |
| Published: |
2024
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| In: |
The European respiratory journal
Year: 2024, Volume: 64, Issue: 3, Pages: 1-5 |
| ISSN: | 1399-3003 |
| DOI: | 10.1183/13993003.00347-2024 |
| Online Access: | Verlag, kostenfrei, Volltext: https://doi.org/10.1183/13993003.00347-2024 Verlag, kostenfrei, Volltext: https://publications.ersnet.org/content/erj/64/3/2400347 
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| Author Notes: | Mustafa Abdo, Frauke Pedersen, Anne-Marie Kirsten, Frederik Trinkmann, Espen E. Groth, Thomas Bahmer, Henrik Watz, Klaus F. Rabe |
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| 245 | 1 | 0 | |a Association of airway inflammation and smoking status with IL-33 level in sputum of patients with asthma or COPD |c Mustafa Abdo, Frauke Pedersen, Anne-Marie Kirsten, Frederik Trinkmann, Espen E. Groth, Thomas Bahmer, Henrik Watz, Klaus F. Rabe |
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| 520 | |a Asthma and COPD are heterogeneous inflammatory airway conditions. Interleukin (IL)-33 is an epithelial pleiotropic cytokine that regulates type 1 and type 2 immune responses [1]. Clinical trials have shown promising efficacy of monoclonal antibodies targeting IL-33 and its ST2 receptor in asthma and COPD [2-4]. So far, little is known about the characterisation of airway inflammation associated with increased IL-33 levels in patients with asthma or COPD. Moreover, previous studies have reported a potential impact of smoking status on IL-33 protein levels [5]. Therefore, we investigated the association of smoking status and airway inflammatory phenotypes with IL-33 levels in patients with asthma or COPD. Such clinical characterisation could provide new insights for selecting patients who might benefit from anti-IL-33 therapy. | ||
| 700 | 1 | |a Pedersen, Frauke |e VerfasserIn |4 aut | |
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| 700 | 1 | |a Groth, Espen E. |e VerfasserIn |4 aut | |
| 700 | 1 | |a Bahmer, Thomas |e VerfasserIn |4 aut | |
| 700 | 1 | |a Watz, Henrik |e VerfasserIn |4 aut | |
| 700 | 1 | |a Rabe, Klaus F. |e VerfasserIn |4 aut | |
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