Apolipoprotein A-I increases the activity of lysosomal glycosidases in the liver of mice with BCG-induced tuberculosis inflammation

Abstract

This work shows the ability of apolipoprotein A-I to influence the activity of lysosomal glycosidases in the liver of mice in a model of BCG-induced tuberculous inflammation. The aim of the investigation was to study the activity of lysosomal glycosidases in the liver of mice using a model of BCG-induced tuberculous inflammation after intravenous administration of apolipoprotein A-I. Material and methods. The studies were performed on male CBA mice weighing 20-22 g. Disseminated tuberculous inflammation was modeled by a single intraperitoneal injection of 0.5 mg of BCG vaccine. The activity of lysosomal glycosidases was assessed spectrofluorimetrically by the content of hydrolysis products of the corresponding fluorogenic substrates. Results. Tuberculous inflammation led to a pronounced decrease in the activity of lysosomal glycosidases in the liver. Thus, β-galactosidase was decreased 2.3 times, β-glucosidase – 2.8 times, β-glucuronidase – 2.5 times compared with healthy animals. Intravenous injection of apolipoprotein A-I to animals against the background of BCG infection prevented a significant decrease in the enzymatic activity of glycosidases and these values practically did not differ from the control values. Conclusions. Enzymatic activity of lysosomal glycosidases in the group of mice with intravenous administration of apolipoprotein A-I against the background of BCG infection was 1.5–2 times higher than the corresponding indicators in the group of animals with BCG-infection without administration of apolipoprotein A-I, i.e. without treatment.

Mechanism of lungs fibrosis in mycobacterial infection

“…This mechanism, according to the authors, underlies fibrosis associated with granuloma. To some extent, the mechanism of MMT can explain the data on a significant increase in the volume density of collagen fibers in the granuloma within a month after infecting (22 times) relative to the number of fibroblasts in the granuloma, which increased only 5 times [15]. Granulomas recruit inflammatory dendritic cells that can regulate local T-cell responses and may play a direct role in the spread of granulomatous inflammation [38].…”

“…Traditionally, lung fibrosis has been considered a result of predominantly chronic inflammation [12][13][14]. However, as shown in an experiment on a mice model of Mycobacterium bovis bacillus Calmette-Guérin (BCG)-induced generalized inflammation, fibrosis develops early, more precisely, 3 days after infecting, even before the development of destructive processes in the organ and chronic inflammation [15]. A month after infection, the numerical density of BCG granulomas increased by 5 times, their diameter by 6 times, the volume density of collagen fibers in lung tissue and in granuloma by 14 times and 22 times, respectively, the number of fibroblasts in the granuloma by 5 times.…”