Content of Th17 related and Th2 cytokines in asthma patients with cold airway hyperresponsiveness

The phenomenon of cold airway hyperresponsiveness is rather common among patients with bronchial asthma. Possible participation of immune mechanisms in its occurence is scarcely studied. In particular, there is no information about interaction between Th17-related cytokines, and cytokines of Th2 immune response related to inflammation in asthma patients with cold-induced bronchospasm.Our objective was to evaluate the contents of IL-17A, IL-6, IL-22, IL-4 and IL-13 interleukins in asthma patients, and to specify their role in the formation of cold airway hyperresponsiveness. Spirometric indices of forced expiratory flow were measured in 43 patients with bronchial asthma. The content of interleukins in blood serum was estimated before and after bronchoprovocation test with 3-min. isocapnic hyperventilation with cold (-20 °C) air. Two groups of patients were formed with presence (group 1, n = 14) and absence (group 2, n = 29) of cold airway hyperresponsiveness, verified by the degree of forced expiratory volume reduction per 1 sec. (∆FFV 1ihca ) after the cold test (-16.5 (-20.0 – -12.0)% and -2.3 (-3.5 – -0.8)%, respectively; p < 0.0001). In group 1, when compared with group 2, lower baseline values of FEV 1 (88.1±3.1% and 96.6±2.2%, p = 0.044), and forced midexpiratory flow (MEF 25-75 62.4±3.87% and 75.6±3.7%, p = 0.013) were registered. Moreover, the baseline contents of IL-17A, IL-6, IL-4 in subjects with cold airway hyperresponsiveness were significantly higher than in patients who did not respond to cold air. There was a correlation between IL-17A content in blood and severity of bronchial reaction (∆FEV 1ihca ) to cold test (Rs = -0.33; p = 0.049). In asthma patients with cold airway hyperresponsiveness, high contents of IL-17A, IL-6 and IL-4 suggest a participation of both Th2 and Th1/Th17 cytokines in regulation of cold-induced bronchospasm and immune response with development of immune inflammation of “Th2 low” subtype.