ИММУНОВОСПАЛИТЕЛЬНЫЕ МЕХАНИЗМЫ ФОРМИРОВАНИЯ ХРОНИЧЕСКОГО ПЫЛЕВОГО БРОНХИТА У ШАХТЕРОВ

Abstract

Among the occupational diseases of workers in the main professions of the coal industry, diseases of the respiratory system are quite common, the key role in the formation of which is played by the immune system. The need to study the pathogenesis is due to the fact that the early manifestations of the development of occupational pathology remain invisible.

Purpose of the study – on the basis of clinical studies, to study the immune-inflammatory mechanisms of the formation of chronic dusty bronchitis.

Materials and methods. 435 miners working in underground conditions with dust content in their workplaces exceeding the maximum permissible concentration were examined. The main group consisted of 346 workers with a previously established diagnosis of chronic dust bronchitis. The comparison group was formed of 89 miners without an established diagnosis of respiratory pathology, working in similar sanitary and hygienic conditions.

Main results. Miners with chronic dust bronchitis showed suppression of the main indicator of humoral immunity, as well as the phagocytic activity of neutrophils, which leads to the addition of infection of the bronchopulmonary system and an increase in the severity of inflammation. With the formation of respiratory failure, there is a more pronounced inhibition of the indicators of humoral immunity (a decrease in the level of immunoglobulin G) and the phagocytic activity of neutrophils. A particularly pronounced immunosuppressive effect of hypoxia on humoral immunity is manifested in patients with grade 2 DN, which leads to the addition of an infection of the bronchopulmonary system and an increase in the level of inflammation activity. At the same time, a kind of vicious circle is formed: the infection increases the inflammation and the degree of respiratory failure; under the influence of hypoxia, secondary immune deficiency develops, which contributes to the infectious and inflammatory process in the bronchopulmonary system. Clinically, this is manifested by the fact that patients with chronic dust bronchitis may have no respiratory failure for a long time, which develops and progresses rapidly if an infection of the bronchopulmonary system joins.

In patients without respiratory failure, the preventive and, apparently, compensatory factor is an increase in the activity of interleukin-4, which inhibits the activity of macrophage inflammation and, as a result, slows down the processes of fibrosis in the bronchopulmonary system, which contributes to long-term compensation of the functional state of the respiratory system.

Conclusions. The study in a clinical setting of the immune-inflammatory mechanisms of the formation of chronic dusty bronchitis demonstrates the suppression of humoral immunity and phagocytic activity of neutrophils, which leads to the addition of infection of the bronchopulmonary system and an increase in the severity of inflammation. The same mechanisms are observed during the formation of respiratory failure, which forms a vicious circle: hypoxia has a pronounced immunosuppressive effect, which increases the risk of infection, aggravates inflammation and intensifies respiratory failure. There is a compensatory factor in patients without respiratory failure in the form of an increase in the activity of interleukin-4.