Loss of IL-33 enhances elastase-induced and cigarette smoke extract-induced emphysema in mice
Abstract Background: IL-33, which is known to induce type 2 immune responses via group 2 innate lymphoid cells, has been reported to contribute to neutrophilic airway inflammation in chronic obstructive pulmonary disease. However, its role in the pathogenesis of emphysema remains unclear. Methods: We determined the role of interleukin (IL)-33 in the development of emphysema using porcine pancreas elastase (PPE) and cigarette smoke extract (CSE) in mice. First, IL-33−/− mice and wild-type (WT) mice were given PPE intratracheally. The numbers of inflammatory cells, and the levels of cytokines and chemokines in the bronchoalveolar lavage (BAL) fluid and lung homogenates, were analyzed; quantitative morphometry of lung sections was also performed. Second, mice received CSE by intratracheal instillation. Quantitative morphometry of lung sections was then performed again. Results: Intratracheal instillation of PPE induced emphysematous changes and increased IL-33 levels in the lungs. Compared to WT mice, IL-33−/− mice showed significantly greater PPE-induced emphysematous changes. No differences were observed between IL-33−/− and WT mice in the numbers of macrophages or neutrophils in BAL fluid. The levels of hepatocyte growth factor were lower in the BAL fluid of PPE-treated IL-33−/− mice than WT mice. IL-33−/− mice also showed significantly greater emphysematous changes in the lungs, compared to WT mice, following intratracheal instillation of CSE. Conclusion: These observations suggest that loss of IL-33 promotes the development of emphysema and may be potentially harmful to patients with COPD..
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Preprint| Erscheinungsjahr: |
2022 |
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| Erschienen: |
2022 |
| Enthalten in: |
ResearchSquare.com - (2022) vom: 28. Juli Zur Gesamtaufnahme - year:2022 |
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| Sprache: |
Englisch |
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| Beteiligte Personen: |
Morichika, Daisuke [VerfasserIn] |
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| doi: |
10.21203/rs.3.rs-52288/v1 |
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| PPN (Katalog-ID): |
XRA034688730 |
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| 520 | |a Abstract Background: IL-33, which is known to induce type 2 immune responses via group 2 innate lymphoid cells, has been reported to contribute to neutrophilic airway inflammation in chronic obstructive pulmonary disease. However, its role in the pathogenesis of emphysema remains unclear. Methods: We determined the role of interleukin (IL)-33 in the development of emphysema using porcine pancreas elastase (PPE) and cigarette smoke extract (CSE) in mice. First, IL-33−/− mice and wild-type (WT) mice were given PPE intratracheally. The numbers of inflammatory cells, and the levels of cytokines and chemokines in the bronchoalveolar lavage (BAL) fluid and lung homogenates, were analyzed; quantitative morphometry of lung sections was also performed. Second, mice received CSE by intratracheal instillation. Quantitative morphometry of lung sections was then performed again. Results: Intratracheal instillation of PPE induced emphysematous changes and increased IL-33 levels in the lungs. Compared to WT mice, IL-33−/− mice showed significantly greater PPE-induced emphysematous changes. No differences were observed between IL-33−/− and WT mice in the numbers of macrophages or neutrophils in BAL fluid. The levels of hepatocyte growth factor were lower in the BAL fluid of PPE-treated IL-33−/− mice than WT mice. IL-33−/− mice also showed significantly greater emphysematous changes in the lungs, compared to WT mice, following intratracheal instillation of CSE. Conclusion: These observations suggest that loss of IL-33 promotes the development of emphysema and may be potentially harmful to patients with COPD. | ||
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| 700 | 1 | |a Oda, Naohiro |e verfasserin |4 aut | |
| 700 | 1 | |a Fujii, Utako Fujii Utako |e verfasserin |4 aut | |
| 700 | 1 | |a Senoo, Satoru |e verfasserin |4 aut | |
| 700 | 1 | |a Itano, Junko |e verfasserin |4 aut | |
| 700 | 1 | |a Kitaguchi, Yoshiaki |e verfasserin |4 aut | |
| 700 | 1 | |a Yasuo, Masanori |e verfasserin |4 aut | |
| 700 | 1 | |a Hanaoka, Masayuki |e verfasserin |4 aut | |
| 700 | 1 | |a Satoh, Takashi |e verfasserin |4 aut | |
| 700 | 1 | |a Akira, Shizuo |e verfasserin |4 aut | |
| 700 | 1 | |a Kiura, Katsuyuki |e verfasserin |4 aut | |
| 700 | 1 | |a Maeda, Yoshinobu |e verfasserin |4 aut | |
| 700 | 1 | |a Miyahara, Nobuaki |e verfasserin |4 aut | |
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