Reactive and destructive changes of Peyer’s patches in rats with experimental burn disease under infusion of detoxification solutions
Authors: Cherkasov V.G. , Matkivska R.M. , Cherkasov E.V. , Kaminskyi R.F. , Yaremenko L.M. 
Published: March 2020

The pathogenesis of burn immune dysfunction and burn enteropathy needs further clarification given that the cellular lesions of lymphoid tissue associated with mucous membranes are the least studied. The purpose of the study was to establish reactive and destructive changes in Peyer’s patches of rats after burn injury of the skin with the use of intravenous infusion of isotonic sodium chloride solution and combined colloid-hyperosmolar solutions. White male rats weighing 160-200 g at 6 months of age were divided into 4 groups (18 animals in each group): I, II, III – rats with burn skin injury (grade II-III burn with an area of 23% of body surface area and the development of moderate-severity shock state) which was administered a separate intravenous infusion once a day for the first 7 days of the experiment with isotonic sodium chloride, lactoprotein with sorbitol and HAES-LX-5%, in each case at a dose of 10 ml/kg; IV – intact animals. The material was collected from rats under deep thiopental intraperitoneal anesthesia after 1, 3, 7, 14, 21 and 30 days after burn injury. Biopsies from Peyer’s patches for histological and electron microscopic examination were processed using conventional methods. Investigation of histological preparations stained with hematoxylin-eosin was performed on an Olympus BX51 microscope. Ultrathin sections were contrasted on copper support meshes with uranyl acetate and lead citrate according to Reynolds and studied using a PEM-125K electron microscope. Electron and light microscopy data indicate that intravenous infusion of colloidal-hyperosmolar solutions (lactoprotein with sorbitol and HAES-LX-5%) promotes suppression of inflammatory response, inhibits necrosis, and optimizes lymphoid apoptosis at Peyer’s patches of rats with experimental burn disease caused by burn injury to the skin of 21-23% of the body surface. Apoptotic lymphocytes and their apoptotic bodies are effectively phagocytosed by macrophages and are digestible in heterophagolysosomes. The apoptotic altered dendritic cells in Peyer’s patches are characterized by osmiophilic cytoplasm and a nucleus with high electron density amorphous nucleoplasm. In the cytoplasm are located mitochondria with enlightened matrix and destroyed cristae, irregularly expanded tubules of variable configuration of a granular endoplasmic reticulum with electronically transparent content and numerous derivatives of their vacuole transformation, which are sharply darkened. The fusion of vacuoles leads to the formation of large electron-luminous cavities filled with various residues of compacted degraded cellular structures. Vacualization promotes site segmentation of condensed cytoplasm of apoptotic dendritic cells and formation of apoptotic blebs, which are subject to entrapment and subsequent sequential degradation with the participation of neighboring macrophages. The structural changes of the organelles of the protein-synthesizing apparatus found in Peyer’s plaque cells in rats with experimental burn disease can be regarded as a manifestation caused by functional overload of the granular endoplasmic reticulum (ER-stress). The consequence of optimal development of ER-stress and subsequent unfolded protein response is the apoptotic degradation of the corresponding cell, the course of which is modified by the use of colloid-hyperosmolar solutions.