When an allergen first comes in contact with the mucosa, it damages the epithelial barrier, which triggers cytokine secretion, including TSLP, IL-25 and IL-33. In the presence of cytokines, the secondary contact with the allergen induces maturation of dendritic cells (DCs) and their migration to lymph nodes, where DCs in collaboration with major histocompatibility complex molecules (MHC-II) “report” the allergen to Th0 cells (T-helpers) initiating their proliferation and differentiation into Th2 cells. Activated allergen-specific Th2s produce a wide range of cytokines: IL-4 (increases proliferation of B-lymphocytes and serves as their growth and differentiation factor, induces B-cell class switching to IgE), IL-5 (stimulates proliferation of eosinophils and facilitates release of the major basic protein) and IL-9 (activates mast cells). Allergen-specific IgE antibodies bind to high-affinity receptors (FceRI) of mast cells and basophils and to low- affinity receptors (FceRII) of eosinophils and macrophages. In case of a repeated allergen invasion, IgE of mast cell membranes binds to the allergen, thus ensuring its degranulation. Not all pathogens can be eliminated by antimicrobial peptides if bacterial load is high. Part of them is recognized by epithelial TLRs of the respiratory tract sustaining bronchial inflammation.

Note. Data are presented as a median (25 %; 75 %) of cDNA copies per 1 million copies of cDNA of β-actin, p <0.05