Impact of cigarette smoke and il-17a activation on asthmatic patients with chronic rhinosinusitis*

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.