Dynamics of signs of granulomatous inflammation of the liver after administration of the BCG vaccine in mice of different ages

Abstract

Purpose of the study. The aim of the study was to study the morphogenesis of granulomatous inflammation in the liver in newborn animals and in remote periods of life.Materials and methods. The experiment was carried out on 70 newborn C57BL / 6 mice, divided into two groups. On the first day after birth, mice of the 1st (experimental) group were injected intraperitoneally with a solution of the BCG vaccine at a dose of 0.02 mg / kg. On the fi rst day of the beginning of the experiment, the mice of the 2nd (control) group were injected intraperitoneally with 0.02 ml of physiological solution. Liver samples were subjected to morphological and morphometric study: the body weight of mice (g), the volumetric density (Vv) of dystrophy and necrosis of hepatocytes, foci of extramedullary hematopoiesis, the number density (Nai) of binuclear hepatocytes, mitotic figures, the diameter of granulomas (μm), and the number density were calculated (Nai) granulomas in test area.Results. The introduction of the BCG vaccine to newborn mice on the 1st day led to a delay in their development and a lack of body weight. With the introduction of the BCG vaccine to newborn mice of the C57B1 / 6 line, a delayed formation of granulomas is noted, starting from the 10th day after the administration of the BCG vaccine, and a subsequent increase by 56 days in both the number and size of granulomas. The foci of extramedullary hematopoiesis in the liver of mice after the administration of the BCG vaccine persist for a longer period (up to 28 days), which is probably due to the participation of cells of the foci of hematopoiesis in the inflammatory process in the liver parenchyma. With the introduction of the BCG vaccine, pronounced destructive changes in hepatocytes in mice at all age periods are noted with reduced rates of reparative liver regeneration. Conclusion. The introduction of BCG vaccine to newborn mice led to the formation of tuberculous granulomas in the liver during the adult period of life with the development of destructive changes in hepatocytes and a reduced reparative ability of the liver.