Association between cigarette smoking and interleukin-17A expression in nasal tissues of patients with chronic rhinosinusitis and asthma

Abstract

Cigarette smoke plays a substantial role in the development of airway inflammatory diseases, including asthma and chronic rhinosinusitis (CRS). Interleukin (IL)-17A might contribute to cigarette smoke-related inflammation of the airway. This study aimed to investigate the association between cigarette smoking and IL-17A expression in the nasal tissues of patients with CRS and asthma.We prospectively recruited 24 patients (13 smokers, 11 nonsmokers) with CRS and asthma and 6 patients with asthma but without CRS (control group) in a tertiary medical center. Nasal mucosa was obtained as part of the nasal surgery. Protein and mRNA levels of IL-17A in the nasal tissues were determined by immunostaining and real-time polymerase chain reaction.The number of unexpected emergency clinic visits for acute asthma attacks were higher among smokers than among nonsmokers. Interleukin-17A protein and mRNA levels in the nasal tissues of smokers were greater compared to those in the nasal tissues of nonsmokers (P = 0.02 both) and control patients (P = 0.05 and 0.04, respectively).Cigarette smoking was associated with an increase in the number of unexpected emergency clinic visits due to acute asthma attack and in the expression of IL-17A in the nasal tissues of patients with airway inflammatory diseases.

Age‐associated changes in chronic rhinosinusitis endotypes

“…In our previous study utilizing eosinophilic CRS murine models, smoking exposure enhanced eosinophilic infiltration and generated more severe polypoid remodelling with type 1, 2, and 3 responses up‐regulated . The CRS mucosal cytokine profile of smokers has been reported to be dominated type 3 mediators such as IL‐17A, CXCL‐8, and TNF‐ɑ in earlier studies . Dysregulated host defences such as reduced expression level of the polymeric immunoglobulin receptor, secretory leucocyte protease inhibitor, and the long and short palate, lung and nasal epithelium clone protein were observed when cigarette smoke was exposed .…”

Asthma-COPD overlap syndrome: pathogenesis, clinical features, and therapeutic targets

“…[84][85][86][87][88] This process may be mediated by cytokines, as interleukin (IL)-6, IL-8, and IL-17A have all been implicated in n eutrophil chemotaxis in smokers with asthma. [85][86][87][88][89] In addition, smoking may induce CD8+ T cell proliferation in the asthmatic airway, 90 similar to COPD. 91 92 Studies have shown that both neutrophil and CD8+ T cell numbers correlate well with increasing airflow obstruction.…”

IL17A polymorphism and elevated IL17A serum levels are associated with oral lichen planus

“…Also, IL17A serum levels can be influenced by periodontal disease and smoking status was not assessed in the present study. Although there is no evidence pointing to the influence of smoking on IL17A expression on oral tissues, it was significantly elevated in the bronchial mucosa of asthmatic smokers, supporting its role on the development of neutrophilic inflammation of the airways, characterising severe disease and acute asthma attacks (Huang et al., ; Siew, Wu, Ying, & Corrigan, ). Inasmuch, recent evidence suggests an increase in IL17A mRNA expression in OLP patients with periodontal disease (Linhartova et al., ).…”