Jian-Hui Chen1, Ling Qin2, Ying-Ying Shi3, Jun-Tao Feng4, Yu-Long Zheng5, Yu-Feng Wan6, Chuan-Qin Xu7, Xiao-Mei Yang8, Cheng-Ping Hu9. 1. Department of Respiratory Medicine, Xiangya Hospital of Central South University (Key Site of National Clinical Research Center for Respiratory Disease), Changsha 410008, Hunan Province, China; Department of Respiratory Medicine, Huai'an Second People's Hospital, Huai'an 223002, Jiangsu Province, China. Electronic address: 1284530031@qq.com. 2. Department of Respiratory Medicine, Xiangya Hospital of Central South University (Key Site of National Clinical Research Center for Respiratory Disease), Changsha 410008, Hunan Province, China. Electronic address: 15152368813@163.com. 3. Key Laboratory for Medicinal Exploitation of Huai'an Regional Resource, College of Chemical Engineering, Huaiyin Institute of Technology, Huai'an 223003, Jiangsu Province, China. Electronic address: shiyingying82012@163.com. 4. Department of Respiratory Medicine, Xiangya Hospital of Central South University (Key Site of National Clinical Research Center for Respiratory Disease), Changsha 410008, Hunan Province, China. Electronic address: 513204423@qq.com. 5. Department of Respiratory Medicine, Huai'an Second People's Hospital, Huai'an 223002, Jiangsu Province, China. Electronic address: ha183@163.com. 6. Department of Respiratory Medicine, Huai'an Second People's Hospital, Huai'an 223002, Jiangsu Province, China. Electronic address: ggwanyufeng@163.com. 7. Department of Respiratory Medicine, Huai'an Second People's Hospital, Huai'an 223002, Jiangsu Province, China. Electronic address: 657442476@qq.com. 8. Department of Respiratory Medicine, Huai'an Second People's Hospital, Huai'an 223002, Jiangsu Province, China. Electronic address: ha315@163.com. 9. Department of Respiratory Medicine, Xiangya Hospital of Central South University (Key Site of National Clinical Research Center for Respiratory Disease), Changsha 410008, Hunan Province, China. Electronic address: cjh0517@sohu.com.
Abstract
BACKGROUND: Obesity worsens asthma control partly through enhanced airway neutrophilia, altered lung mechanics and comorbidities, including obstructive sleep apnea syndrome, gastroesophageal reflux disease and depression. Although controversial, obesity may also cause poorer outcomes in acute asthma. IL-17 is associated with neutrophilic inflammation, steroid resistance and severe asthma, but its importance in the association between asthma and obesity is unknown. OBJECTIVE: To investigate the role of IL-17 in obese asthma in both acute and stable settings. METHODS: Both stable (n = 177) and acute (n = 78) asthmatics were recruited and categorized into lean (n = 77 and 39 respectively), overweight (n = 41 and 17 respectively) and obese (n = 59 and 22 respectively) groups and compared for clinical characteristics, including sputum and plasma IL-17 protein concentrations, sputum cellularity, spirometry and comorbidities. Correlations of IL-17 expression with other measures were explored. RESULTS: In stable subjects, airway neutrophilia and IL-17 concentrations were most prominent in the obese, and correlated positively with each other. Significant increase in plasma IL-17 levels was also noted and associated with elevated depressive symptoms in obesity. In acute asthma, IL-17 expression, like most other clinical measures, was similar among lean, overweight and obese groups, but was higher in acute versus stable asthma subjects, with sputum IL-17 correlating positively with sputum neutrophils and negatively with FEV1 and plasma IL-17 showing a positive connection to airway eosinophilia during exacerbation. CONCLUSIONS: IL-17 contributes to worse disease control in obese asthma through enhancing airway neutrophilia and depression, and may implicate in asthma exacerbations. Effects of adiposity on acute asthma remain uncertain. Copyright Â
BACKGROUND:Obesity worsens asthma control partly through enhanced airway neutrophilia, altered lung mechanics and comorbidities, including obstructive sleep apnea syndrome, gastroesophageal reflux disease and depression. Although controversial, obesity may also cause poorer outcomes in acute asthma. IL-17 is associated with neutrophilic inflammation, steroid resistance and severe asthma, but its importance in the association between asthma and obesity is unknown. OBJECTIVE: To investigate the role of IL-17 in obese asthma in both acute and stable settings. METHODS: Both stable (n = 177) and acute (n = 78) asthmatics were recruited and categorized into lean (n = 77 and 39 respectively), overweight (n = 41 and 17 respectively) and obese (n = 59 and 22 respectively) groups and compared for clinical characteristics, including sputum and plasma IL-17 protein concentrations, sputum cellularity, spirometry and comorbidities. Correlations of IL-17 expression with other measures were explored. RESULTS: In stable subjects, airway neutrophilia and IL-17 concentrations were most prominent in the obese, and correlated positively with each other. Significant increase in plasma IL-17 levels was also noted and associated with elevated depressive symptoms in obesity. In acute asthma, IL-17 expression, like most other clinical measures, was similar among lean, overweight and obese groups, but was higher in acute versus stable asthma subjects, with sputum IL-17 correlating positively with sputum neutrophils and negatively with FEV1 and plasma IL-17 showing a positive connection to airway eosinophilia during exacerbation. CONCLUSIONS:IL-17 contributes to worse disease control in obese asthma through enhancing airway neutrophilia and depression, and may implicate in asthma exacerbations. Effects of adiposity on acute asthma remain uncertain. Copyright Â
Authors: Maja A Hofmann; Joachim W Fluhr; Christoph Ruwwe-Glösenkamp; Katarina Stevanovic; Karl-Christian Bergmann; Torsten Zuberbier Journal: Clin Transl Allergy Date: 2021-08-13 Impact factor: 5.871
Authors: Sarah Orfanos; Joseph Jude; Brian T Deeney; Gaoyuan Cao; Deepa Rastogi; Mark van Zee; Ivan Pushkarsky; Hector E Munoz; Robert Damoiseaux; Dino Di Carlo; Reynold A Panettieri Journal: Am J Physiol Lung Cell Mol Physiol Date: 2018-08-30 Impact factor: 5.464