CC16 alleviates PM2.5-induced lung epithelial cell injury and airway inflammation in asthmatic mice by inhibiting ferroptosis
Background: Exposure to PM2.5 represents a significant public health challenge, closely associated with the worsening of asthma, a condition that still lacks effective preventive measures. Club Cell 16 kDa protein (CC16), recognized for its anti-inflammatory and antioxidant properties, may serve a p...
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| Format: | Article |
| Language: | English |
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Elsevier
2025-01-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651324014933 |
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| author | Aili Wang Jianling Liu Zhangwen Li Ze Qian Shuo Yang Shaohua Luo Jinle Lin Jian Wu |
| author_facet | Aili Wang Jianling Liu Zhangwen Li Ze Qian Shuo Yang Shaohua Luo Jinle Lin Jian Wu |
| author_sort | Aili Wang |
| collection | DOAJ |
| description | Background: Exposure to PM2.5 represents a significant public health challenge, closely associated with the worsening of asthma, a condition that still lacks effective preventive measures. Club Cell 16 kDa protein (CC16), recognized for its anti-inflammatory and antioxidant properties, may serve a protective function in asthma exacerbated by PM2.5; however, the underlying mechanisms, particularly those related to ferroptosis, remain poorly understood. Methods: The impact of CC16 on inflammation and ferroptosis was assessed using a TC-1 lung epithelial cell model exposed to PM2.5, as well as an ovalbumin (OVA)-induced asthmatic mouse model also subjected to PM2.5 exposure. Results: CC16 significantly modulated key regulators of ferroptosis (NRF2, GPX4, SLC7A11, HO-1) and attenuated pro-inflammatory cytokines (IL-13, IL-5, IL-6, IL-1β, IL-17A) in PM2.5-exposed lung epithelial cells. Furthermore, it enhanced pulmonary function while reducing airway inflammation and mucus secretion and inhibited ferroptosis in PM2.5-induced asthmatic mice. Conclusion: CC16 demonstrates promise as a therapeutic agent for PM2.5-induced asthma by modulating ferroptosis and alleviating airway inflammation, thereby providing a novel strategy for asthma management. |
| format | Article |
| id | doaj-art-92f938fbde6b451ebf82715bc12edf81 |
| institution | Kabale University |
| issn | 0147-6513 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj-art-92f938fbde6b451ebf82715bc12edf812025-01-23T05:25:28ZengElsevierEcotoxicology and Environmental Safety0147-65132025-01-01289117417CC16 alleviates PM2.5-induced lung epithelial cell injury and airway inflammation in asthmatic mice by inhibiting ferroptosisAili Wang0Jianling Liu1Zhangwen Li2Ze Qian3Shuo Yang4Shaohua Luo5Jinle Lin6Jian Wu7Second Department of Elderly Respiratory, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangdong Provincial Geriatric Institute, Guangzhou, Guangdong 510080, China; Department of Respiratory and Critical Care Medicine, Wuhan No.1 Hospital, Wuhan, Hubei 430022, ChinaSecond Department of Elderly Respiratory, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangdong Provincial Geriatric Institute, Guangzhou, Guangdong 510080, China; School of Medicine, South China University of Technology, Guangzhou, Guangdong 510080, ChinaSecond Department of Elderly Respiratory, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangdong Provincial Geriatric Institute, Guangzhou, Guangdong 510080, China; School of Medicine, South China University of Technology, Guangzhou, Guangdong 510080, ChinaSecond Department of Elderly Respiratory, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangdong Provincial Geriatric Institute, Guangzhou, Guangdong 510080, ChinaDepartment of Respiratory and Critical Care Medicine, Wuhan No.1 Hospital, Wuhan, Hubei 430022, ChinaSecond Department of Elderly Respiratory, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangdong Provincial Geriatric Institute, Guangzhou, Guangdong 510080, ChinaDepartment of Emergency Medicine, Affiliated Baoan Hospital of Shenzhen, The Second School of Clinical Medicine, Southern Medical University, Shenzhen, Guangdong 518101, ChinaSecond Department of Elderly Respiratory, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangdong Provincial Geriatric Institute, Guangzhou, Guangdong 510080, China; Correspondence to: Second Department of Elderly Respiratory, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, and Guangdong Provincial Geriatrics Institute, Guangzhou, Guangdong, China.Background: Exposure to PM2.5 represents a significant public health challenge, closely associated with the worsening of asthma, a condition that still lacks effective preventive measures. Club Cell 16 kDa protein (CC16), recognized for its anti-inflammatory and antioxidant properties, may serve a protective function in asthma exacerbated by PM2.5; however, the underlying mechanisms, particularly those related to ferroptosis, remain poorly understood. Methods: The impact of CC16 on inflammation and ferroptosis was assessed using a TC-1 lung epithelial cell model exposed to PM2.5, as well as an ovalbumin (OVA)-induced asthmatic mouse model also subjected to PM2.5 exposure. Results: CC16 significantly modulated key regulators of ferroptosis (NRF2, GPX4, SLC7A11, HO-1) and attenuated pro-inflammatory cytokines (IL-13, IL-5, IL-6, IL-1β, IL-17A) in PM2.5-exposed lung epithelial cells. Furthermore, it enhanced pulmonary function while reducing airway inflammation and mucus secretion and inhibited ferroptosis in PM2.5-induced asthmatic mice. Conclusion: CC16 demonstrates promise as a therapeutic agent for PM2.5-induced asthma by modulating ferroptosis and alleviating airway inflammation, thereby providing a novel strategy for asthma management.http://www.sciencedirect.com/science/article/pii/S0147651324014933AsthmaFerroptosisAirway epithelial cellPM2.5CC16 |
| spellingShingle | Aili Wang Jianling Liu Zhangwen Li Ze Qian Shuo Yang Shaohua Luo Jinle Lin Jian Wu CC16 alleviates PM2.5-induced lung epithelial cell injury and airway inflammation in asthmatic mice by inhibiting ferroptosis Ecotoxicology and Environmental Safety Asthma Ferroptosis Airway epithelial cell PM2.5 CC16 |
| title | CC16 alleviates PM2.5-induced lung epithelial cell injury and airway inflammation in asthmatic mice by inhibiting ferroptosis |
| title_full | CC16 alleviates PM2.5-induced lung epithelial cell injury and airway inflammation in asthmatic mice by inhibiting ferroptosis |
| title_fullStr | CC16 alleviates PM2.5-induced lung epithelial cell injury and airway inflammation in asthmatic mice by inhibiting ferroptosis |
| title_full_unstemmed | CC16 alleviates PM2.5-induced lung epithelial cell injury and airway inflammation in asthmatic mice by inhibiting ferroptosis |
| title_short | CC16 alleviates PM2.5-induced lung epithelial cell injury and airway inflammation in asthmatic mice by inhibiting ferroptosis |
| title_sort | cc16 alleviates pm2 5 induced lung epithelial cell injury and airway inflammation in asthmatic mice by inhibiting ferroptosis |
| topic | Asthma Ferroptosis Airway epithelial cell PM2.5 CC16 |
| url | http://www.sciencedirect.com/science/article/pii/S0147651324014933 |
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