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22. Pathogenesis of bronchial asthma (BA)

Pathogenesis. Altered bronchial reactivity is the central link in the pathogenesis of the disease and can be primary and secondary. In the first case, the change in reactivity is congenital and acquired. Secondary changes in bronchial reactivity are a manifestation of changes in the reactivity of the immune, endocrine, and nervous systems of the body. Thus, speaking about the pathogenesis of AD, we can distinguish 2 groups of mechanisms: immunological and non-immunological.

Type I (atopic, reaginic, or anaphylactic). In response to the ingestion of exoallergen antigens (pollen, animal and vegetable proteins, bacteria and drugs), an increased production (reagins) occurs, which are fixed and accumulated on mast cells (primary effector cells). This is the immunological stage of AD. Following this, the pathochemical stage of the process develops - degranulation of mast cells with the release of vasoactive, bronchospastic and chemotactic substances (histamine, serotonin, various chemotactic factors, etc.).

Under the influence of biologically active substances, the pathophysiological stage of pathogenesis begins: the permeability of the microcirculatory bed increases, which leads to the development of edema, serous inflammation, and bronchospasm.

Type III reaction (immunocomplex type, or Arthus phenomenon) develops under the influence of exoallergens and endoallergens.

The reaction occurs in the zone of excess antigen with the participation of precipitating antibodies belonging to the immunoglobulins of classes O and M. The damaging effect of the formed antigen-antibody complex is realized through complement activation, the release of lysosomal enzymes.

There is damage to the basal membranes, spasm of smooth muscles of the bronchi, vasodilation, and the permeability of the microvasculature increases.

Type IV (cellular, delayed-type hypersensitivity) is characterized by the fact that sensitized lymphocytes have a damaging effect. In this case, the mediators of the allergic reaction are lymphokines (act on macrophages, epithelial cells), lysosomal enzymes, and an activated kinin system. Under the influence of these substances, edema develops, swelling of the mucous membrane, bronchospasm, hyperproduction of viscous bronchial secretions.

Non-immunological mechanisms are the primary change in bronchial reactivity as a result of congenital and acquired biological defects. Non-immunological mechanisms act on primary or secondary effector cells or on the receptors of the smooth muscles of the bronchi, blood vessels, cells of the bronchial glands. This changes the reactivity of target cells and, above all, mast cells, which is accompanied by excessive production of biologically active substances (histamine, leukotrienes, etc.).

Recently, there has been talk about the special role of glucocorticoid insufficiency and dysovarian disorders in the pathogenesis of bronchial obstruction disorders. Insufficiency of glucocorticosteroids leads to the development of hyperreactivity of mast cells, decreased synthesis of catecholamines, activation of prostaglandins F2a, as well as disruption of the immunocompetent system.

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