General mechanisms of the pathogenesis of bronchial asthma

At present, bronchial asthma is considered as a disease with complex multifactorial pathogenesis, including immune and non-immunological mechanisms: allergic predisposition, immunological damage of various types, disorders of adrenergic and cholinergic regulation, neuroendocrine disorders, bronchial hyperreactivity to various stimuli: mediators of immediate allergy, odors, non-specific dust, smoking), changes in temperature and humidity, mental factors, physical. tension, respiratory infections. These stimuli elicit the same response (airway obstruction) as specific antigens.

The role of genetic factors in the pathogenesis of bronchial asthma

The role of genetic factors in pathogenesis is not fully established. It is assumed that Ir genes are involved in the formation of endogenous bronchial asthma, since they are associated with antiviral immunity. About 80% of patients with endogenous asthma are homozygous for HLA – BW6. In Pi-type heterozygotes (in children and adolescents) an increased frequency of intermediate activity of agantitrnpsin was found.

The role of immunological mechanisms in the pathogenesis of bronchial asthma

Atopic asthma is based on bronchospasm due to reactions dependent on immunoglobulin E. A large number of mast cells are concentrated in the submucosal layer of the bronchi, especially at the level of the peripheral airways, which contributes to the development of anaphylaxis.
With atopic bronchial asthma, violations of immunological homeostasis have been identified that determine the development of an immediate type of allergic reaction: increased synthesis of non-specific immunoglobulin E and antibodies related to immunoglobulins E against antigen; insufficiency of the T-system of immunity with impaired immunoregulation (Tsupressor defect is assumed); defects in local immunity, in particular deficiency of immunoglobulin A secretory; dysfunction of phagocytic cells. Also important is the increased ability of mast cells to fix antibodies related to immunoglobulins E. Anaphylactic antibodies can belong to immunoglobulin G (high-speed anaphylaxis antibodies ), which explains the possibility of anaphylaxis with a low level of immunoglobulin E.
When analyzing the causes of penetration of inhaled allergens into the submucous layer of the bronchi many authors admit the possibility of an initial increase in mucosal permeability in individuals with atony, considering this factor as a necessary condition e development of an allergic reaction. Recently, however, with atopic bronchial asthma, basophils that can migrate from the circulatory bed, and mast cells have been found in the lumen of the bronchi. Perhaps the reaction of the antigen with antibodies fixed on these cells may be the first step in the development of an allergic reaction, and the released mediators increase the permeability of the mucous membrane. This assumption is confirmed experimentally. In some patients with atopic bronchial asthma, airway obstruction develops 412 hours after contact with the antigen (in particular, house dust) and lasts for a day or two. In these cases, the pathogenetic role of immunocomplex reactions involving antibodies related to immunoglobulins E and immunoglobulins G. is assumed. After the formation and fixation of immune complexes, bronchial obstruction can be caused by various factors depending on the biological effects of the components C2, C3a, C5a, C5-C9 complement system. It is assumed that the introductory mechanism for the development of immunocomplex damage is p-cpi, caused by immunoglobulin E, which, causing the release of mediators, increase the permeability of capillary endothelium and contribute to the deposition of immune complexes. This explains the presence of double skin and bronchospastic reactions to an antigen in bronchial asthma. According to modern concepts, late-type allergic reactions can cause antibodies related not only to immunoglobulin G, but also to immunoglobulin E. Mediators of late reactions due to immunoglobulin E are not known. The role of histamine in them is unlikely. The role of the eosinophilic chemotactic anaphylaxis factor, the slow-reacting anaphylaxis substance, neutrophil chemotactic factor, platelet aggregation factor, and calicrein-like substances is discussed. Late inflammatory reactions play an important role in the formation of severe asthma with persistent shortness of breath, prolonged bronchospasm, resistant to bronchodilators; in the pathogenesis of a prolonged inflammatory reaction after the cessation of antigenic stimulation, the role of delayed basophilic hypersensitivity is assumed. One of the ways to stimulate basophils may be to activate the complement of immune complexes with antibodies related to immunoglobulin E. Auto-antibodies (antinuclear, anti-pulmonary, to smooth muscles of the bronchi) are detected in atopic asthma, however, their pathogenetic role has not been established. Antibodies against adrenergic B-receptors of smooth muscles were found, their value in the genesis of primary B-adrenergic blockade is assumed. The immunological mechanisms of infectious-allergic bronchial asthma have been less studied. Numerous clinical observations have confirmed its external connection with acute and chronic infectious and inflammatory diseases of the respiratory tract. However, the question of the formation of bacterial allergies as the main mechanism of infectious-allergic bronchial asthma does not have an unambiguous solution. To date, many foreign researchers do not recognize the allergic nature of infectious bronchial asthma. Many years of work by domestic scientists have shown that the pathogenesis of infectious bronchial asthma is based on an allergy to opportunistic and saprophytic microorganisms, most often to neysseries and Staphylococcus aureus. Nonpathogenic neisseria are of particular importance in connection with the alleged antigenic similarity with lung tissue. Neisseria can significantly aggravate the allergenic effect of other microorganisms. There is also information about the identification of allergies to influenza virus and hemophilic bacillus. The following facts are given as evidence of the role of bacterial allergy in the pathogenesis of bronchial asthma: reproduction of bronchospastic reactions in patients using a specific antigen; the occurrence of bronchospastic reactions after allergic diagnostic tests of intradermal microbial allergens; cases of exacerbation of bronchial asthma in the process of hypersensitivity; a specific therapeutic effect of immunotherapy with microbial allergens; the possibility of passive transfer of bacterial sensitization with serum according to Prausnitz-Kustner, in particular with allergies to Neisseria catarrhalis. It is believed that simultaneously developing GNT and HRT are involved in the formation of an infectious allergy in bronchial asthma. One of the evidence of this is various bronchospastic reactions to the antigen: early, occurring within 1 

local_offerevent_note January 8, 2020

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