Chien-Chia Huang1,2, Ta-Jen Lee1,3, Chi-Che Huang1,2, Po-Hung Chang1,2, Chia-Hsiang Fu1,2, Pei-Wen Wu1,4, Chun-Hua Wang5. 1. Division of Rhinology, Department of Otolaryngology, Chang Gung Memorial Hospital and Chang Gung University, Taoyuan, Taiwan 2. Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taiwan 3. Department of Otolaryngology, Xiamen Chang Gung Hospital, Xiamen, China 4. Department of Otolaryngology–Head and Neck Surgery, Chang Gung Memorial Hospital and Chang Gung University, Keelung, Taiwan 5. Department of Thoracic Medicine, Chang Gung Memorial Hospital and Medicine of College, Chang Gung University, Taoyuan, Taiwan
Abstract
Background: Cigarette smoke have adverse effects in the control of asthma and chronic rhinosinusitis (CRS). Interleukin (IL)-17A, the signature cytokine of helper T 17 cells and group 3 innate lymphoid cells (ILC3), has been reported to link with resistance to therapy in airway inflammation. This study aimed to investigate the impact of cigarette smoking and IL-17A activation on the clinical outcomes of asthmatic patients with chronic rhinosinusitis. Methods: 33 patients with CRS and asthma, including 15 smokers and 18 non-smokers, and 7 asthmatic patients without CRS and smoking were prospectively recruited. The Sino-Nasal Outcome Test-22 and Asthma Control Test were used to evaluate sinonasal symptoms and the level of asthma control, respectively. Real-time PCR and immunostaining were applied to evaluate the expression levels of IL-17A and associated immunological factors on surgically-obtained nasal tissues. Results: Nasal surgery improved both sinonasal symptoms and asthma control. Compared to non-smokers, smokers showed poorer improvement in asthma control. The expression of IL-17A, IL-22, aryl hydrocarbon receptor (AhR), and ILC3 was increased in the nasal tissues of smokers with asthma and CRS. The expression of IL-17A mRNA was correlated with that of AhR and with positive nuclear AhR-AhR nuclear translocator staining cells, and that of cyclooxygenase-2 enzyme (COX-2). ILC3 cells were associated with IL-17A, IL-22, AhR, and COX-2 mRNA expression. Conclusions: Cigarette smoking was related to lesser improvement in asthma control after nasal surgery and to IL-17A activation in the nasal tissues of patients with inflammatory airways.
Background: Cigarette smoke have adverse effects in the control of asthma and chronic rhinosinusitis (CRS). Interleukin (IL)-17A, the signature cytokine of helper T 17 cells and group 3 innate lymphoid cells (ILC3), has been reported to link with resistance to therapy in airway inflammation. This study aimed to investigate the impact of cigarette smoking and IL-17A activation on the clinical outcomes of asthmatic patients with chronic rhinosinusitis. Methods: 33 patients with CRS and asthma, including 15 smokers and 18 non-smokers, and 7 asthmatic patients without CRS and smoking were prospectively recruited. The Sino-Nasal Outcome Test-22 and Asthma Control Test were used to evaluate sinonasal symptoms and the level of asthma control, respectively. Real-time PCR and immunostaining were applied to evaluate the expression levels of IL-17A and associated immunological factors on surgically-obtained nasal tissues. Results: Nasal surgery improved both sinonasal symptoms and asthma control. Compared to non-smokers, smokers showed poorer improvement in asthma control. The expression of IL-17A, IL-22, aryl hydrocarbon receptor (AhR), and ILC3 was increased in the nasal tissues of smokers with asthma and CRS. The expression of IL-17A mRNA was correlated with that of AhR and with positive nuclear AhR-AhR nuclear translocator staining cells, and that of cyclooxygenase-2 enzyme (COX-2). ILC3 cells were associated with IL-17A, IL-22, AhR, and COX-2 mRNA expression. Conclusions: Cigarette smoking was related to lesser improvement in asthma control after nasal surgery and to IL-17A activation in the nasal tissues of patients with inflammatory airways.
Authors: Kijeong Lee; In Hak Choi; Hoyoung Lee; Soojeong Choi; Sang Hag Lee; Tae Hoon Kim Journal: Int J Environ Res Public Health Date: 2020-11-09 Impact factor: 3.390