摘要：

The expression profile of various genes in epithelial cells of the bronchi will enable the diagnosis of molecular subphenotypes ofasthma: a) asthma with strong features of Th2 infl ammation, b) asthma with weak features of Th2 infl ammation, and c) asthma without features of Th2 infl ammation. The analysis of the overall gene expression gave three pathognomonic genes, i.e. IL-13 inducible genes in bronchial epithelial swab: periostin, chloride channel regulator 1 (CLCA1) and serpin peptidase inhibitor, clade B (SERPINB2), which may serve as surrogate markers of Th2 inflammation. The gene whose expression diff ers most in asthma with strong features of Th2 infl ammation and asthma with weak features of Th2 infl ammation is CCL26 (eotaxin-3). Pathophysiological mechanisms, which act via IL-25, IL-33 and TSLP (thymic stromal lymphopoietin), underlie asthma without features of Th2 infl ammation and a weak response to the currently available antiasthmatic therapy. The need to identify a phenotype of the disease is the greatest in patients with severe asthma and those with asthma refractory to therapy. Severe asthma could be also diagnosed by determining the genetic profi le of alveolar macrophages from induced sputum. The predictor of FEV1 growth after the administration of anti-IL-13 monoclonal antibody is a combination of serum periostin with NO fraction in exhaled air (FeNO). The combination of urinary leukotriene E4 with FeNO, i.e. their ratio, proved to be a good biomarker of therapy efficiency in asthma. Urinary bromotyrosine could be a marker of asthma control and a predictor of asthma exacerbations in children. In the future, the treatment of asthma will be based on pharmacogenetic findings. In clinical medicine, there is only one biosimilar drug, i.e. omalizumab (monoclonal antibody, serum IgE blocker), authorised for use in patients with severe allergic asthma.

展开