Взаимосвязь альвеолярно-бронхиолярных нарушений с уровнем интерлейкина-20 у больных с внебольничной пневмонией

Abstract

Objective is to study the relationship between clinical, laboratory and radiological manifestations of alveolar-bronchiolar dysfunction with the production of interleukin-20 in patients with community-acquired pneumonia. Materials and methods. We examined 60 patients of both sexes aged 18 to 45 years with bacterial community-acquired pneumonia in the first 3 days of the disease, as well as 15 practically healthy individuals. The material of the study was venous blood, in the serum of which the concentration of interleukins (IL) was determined: IL-1β, -2, -4, -8, -10, -17A, -20, -28A, -33, tumor necrosis factor-alpha (TNFα), interferon-gamma (IFNγ), Clara cell protein (CCP), surfactant protein D (SP-D), prostacyclin (PgI2), soluble form of the Fas-receptor (sFas), and its ligand (sFasL), leukotriene D4 (LTD4), thromboxane A2 (TA2). Results. The development of pneumonia is accompanied by an increase in the production of the studied mediators, which is more pronounced in patients with a severe course of the disease. An increase in the concentration of IL-20 from the minimum to the maximum level is accompanied by a significant proportional decrease in the concentration of IL-1β, TNFα, IL-33, TA2, LTD4, Fas, FasL. A high level of IL-20 was associated with a decrease in the concentration of CCP, indicating a weakening of the alveolar-bronchiolar dysfunction and a decrease in the intensity of the inflammatory reaction in the lung tissue. It was also found that a high level of IL-20 was associated with increased production of PgI2, IFNγ, IL-1RA, IL-17A, IL-8, IL-4, IL-28A, IL-10, SLPI. Conclusion. The results of the study indicate the important role of IL-20 in the development of inflammation of the lower respiratory tract, which consists in regulating the activity of the acute phase response, modulating the production of prostacyclin and leukotrienes, determining the limitation of alveolar-bronchiolar dysfunction in patients with pneumonia, as well as the restriction of proapoptogenic influences that determine the decrease in volumes. tissue and cellular damage in such patients.