Cytokin regulation of local immune reactions in pulmonary tissues (IL-10, IL-4, TGFb1, TNFα), and morphology of the vascular bed and alveolar epithelium of the lung air compartments were studied in a 15-day tail-suspended Wistar male rats with a body mass of 180–200 grams. Cytokin regulation of the local immunity after suspension was characterized by activation of cell proliferation and differentiation regulator TGFβ1 aimed to forestall the inflammatory and auto immune processes and to promote remodeling of the lung epithelial structure and extracellular matrix.
Introduction. Morphological studies of animals (trachea, bronchi, lungs) exposed to the combined inhalation of chemicals in low concentrations showed the progression of structural changes, indicating the activation of inflammation and fibrosis in the lungs. The role of cytokine markers in developing inflammatory and fibrotic processes and remodeling lung tissue has been studied. Materials and methods. Male rats (180-200 g) were exposed to a mixture of chemicals (acetone, acetaldehyde, benzene) in low concentrations of 0.7-1.5; 0.9-1.4; 0.2-0.4 (mg/m3), respectively. The concentrations of IL-6, IL-10, IL-1b, IL-4, TGFβ1, TNFα cytokines (pg/ml) have been measured in the lung homogenate by enzyme-linked immunosorbent assay (ELISA). Microscopic anatomy of the lungs, tracheal wall, bronchi has been studied on the 30th day of exposure and the 15th and 90th days of the recovery period. Results. An increase in interleukin-4 and transforming growth factor TGFβ1 in the homogenate of the lung tissue was shown. An increase in lymphatic follicles, the number of lymphocytes, neutrophils, macrophages, and focal accumulations of eosinophils has been observed in the tracheal wall. In lymphoid infiltrates of the lung tissue - eosinophils, macrophages, and plasmocytes. Accumulation of eosinophilic exudate has been observed in some alveoli. The 90th day of the recovery period is characterized by a significant increase of TGFβ1 in the lung tissue, indicating fibrosis, as evidenced by the rise in the number of fibroblasts between the alveoli in the atelectasis zones of lungs. Conclusion. The chronic combined exposure to the mixture of chemicals in low concentrations is accompanied by a pro-inflammatory process in the lungs with the type II hypersensitivity and increasing IL-4 and TGFβ1 (a key mediator of profibrotic activity).
Purpose: The integrated research of the reaction of the hematopoietic system, including hematopoietic, metabolic changes in the cells and modify their antioxidant capacity during the recovery period after radiation exposure at doses and concentrations that are typical for interplanetary flight: 1) in isolation, i.e. without any external influence; 2) under the influence of negatively ionized air.
Material and methods: The study was conducted on sexually mature mice of line F1(CBA×C57BL6) subject to the rules and regulations of biomedical ethics on the basis of SSC RF IBMP RAS. The pilot study included 2 stages: 1) fractionated γ-irradiation (350 cGy) with the duration of 63 days; 2) the recovery period, lasting 28 days, during which the animals were exposed to negatively ionized air (daily for 70 min). Studied cytological, morphological, biochemical parameters of hematopoiesis: the total number of nucleated cells (bone marrow); the amount of production of erythrocytes, reticulocytes, hemoglobin (in peripheral blood); the content of ATP, lactate, glutathione, activity of glucose-6-phosphate dehydrogenase (G6PD), lactate dehydrogenase (LDH) (in erythrocyte); the ratio and amount of lipid fractions (in the membrane of erythrocytes).
Results: The biological effect of the impact of negatively ionized air on the course of reparative processes in the body after gamma irradiation consists in the accelerated recovery of the number of peripheral blood cells and in a more pronounced degree of myeloid growth, due to:
• increase in the rate of recovery of energy production processes (increase in LDH activity, improvement of lactate and ATP, and more pronounced normalization of oxidation-reduction processes), which facilitates recapitalization of cells with lipid membrane saturation with membrane cholesterol.
• membrane-protective effect of negatively ionized air, based on the restoration of the membrane potential of cells expressing negative effects of blood cells;
• increased life span of cells in peripheral blood and smaller values of the half-life of granulocytes from the bloodstream in the tissue.
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