Allergic bronchial asthma is based on an immediate type allergic reaction due to the interaction of the allergen with specific IgE fixed on the surface of mast cells . The synthesis of specific IgE is carried out by B-lymphocytes , and T-lymphocytes regulate .
Most allergens that cause asthma are airborne allergens. For the development of sensitization , prolonged contact with a large dose of allergen is necessary. In a sensitized patient, even a negligible amount of allergen can cause a severe attack.
The share of allergic bronchial asthma accounts for probably 25 to 35% of all cases. In about a third of patients, mixed bronchial asthma is observed , in which allergy serves as an auxiliary pathogenetic mechanism. Allergic bronchial asthma is more often observed in children and young people and usually proceeds with seasonal exacerbations.
The absence of a connection between exacerbations and the season is observed with allergies to animal hair , feathers and feathers of birds , mites , molds and other allergens that are constantly present in the air.
In most patients, in response to contact with an allergen, reversible bronchial obstruction (the so-called immediate asthmatic reaction) develops within a few minutes. At 30-50%, after 6-10 hours, re-obstruction occurs, in such cases they speak of a double (immediate and delayed) reaction. In very few patients, only a delayed asthmatic reaction is observed. Previously, it was believed that it was she who played the main role in the formation of increased bronchial reactivity, but further studies did not confirm this.
Air allergens , being very small particles, overcome protective barriers, reach the trachea and large bronchi and interact with mast cells interspersed between cells of the ciliated epithelium. A hypothesis explaining how allergens interact with mast cells located in the submucosal layer; today does not exist.