Levels of IL-17A and MMP-9 in induced sputum from patients with asthma and the relationship to the airway inflammation

Abstract

Objective To explore the characteristics and the possible mechanisms of the airway inflammation and airway remodeling.Methods Airway cells were obtained by sputum induction from 15 healthy and 41 asthmatic individuals to processed for cell differentiation, and the supernatant wasassayed for the levels of IL-17A, IL-8, MMP-9.Results The percentage of sputum neutrophils and eosinophils were significantly elevated in patients with severe asthma[(62.6±15.7)%, (8.2±3.9)%]compared to patients with mildasthma[(42.3±18.7)%, (4.9±3.4)%]and healthy controls[(26.3±10.3)%, (1.0±0.8)%](P<0. 05), and the percentage of sputum eosinophils had no significant difference in patients with severe asthma compared to patientswith moderate asthma[(5.4±3.3)%](P<0.05).The levels of sputum IL-17A were significantly elevated in patients with severe asthma[(26±162)pg/ml] compared to patients with mild asthma[(15±91)pg/ml] and healthy controls[(5±23)pg/ml](P<0.05), moreover, those in mild, moderate[(196±103)pg/ml] and severe group were significantly increased compared to patients with healthy controls(P<0.01). As compared to patients with mild and moderate asthma[(166±99)ng/ml,(189±110)ng/ml] and the normal controls[(158±109)ng/ml],the levels of MMP-9 in severe asthma[(451±251)ng/ml] was significantly increased(P<0.01).The sputum level of IL-8 in mild, moderate and severe asthma[(387±227)pg/ml,(390±194)pg/ml, (480±217)pg/ml]was significantly higher than those in normal controls[(203±104)pg/ml](P<0.01). The percentage of sputum neutrophils positively correlated with the levels of IL-17A,IL-8,MMP-9(γ=0.323, P<0.01;γ=0.493, P<0.01;γ=0.344,P<0.05).Conclusions Neutrophilic infiltration in the airways is prominent in severe asthma exacerbations and may contribute to severe airway inflammation and airway wall remodeling in asthma. The inflammatory mediators network consist of IL-17A,IL-8 and MMP-9 plays a potential role in the initiation or maintenance of inflammatory responses. Key words: Asthma; Interleukin-17; Matrix metalloproteinase-9; Airway inflammation