The study in mouse model of BCG-induced granulomatous inflammation showed that early pulmonary fibrosis (day 3-30 postinfection) in tuberculous inflammation was primarily determined by increased number of fibroblasts in the lung interstitium and granulomas and enhanced fibroplastic activity. Fibroplastic processes are initiated via an increase in secretory activity of activated granuloma macrophages caused by the persistence of the pathogen in the cells of the mononuclear phagocytic system. The dynamics of hydroxyproline concentration under these conditions is determined by changes in the number and differentiation degree of fibroblasts in granulomas and lung interstitium at various stages of tuberculous inflammation.

Structure of proteoglycans in the lungs and total glycosaminoglycan content in blood serum were studied on mouse model of BCG-induced granulomatous inflammation in mice (without destructive processes in the lung parenchyma and granulomas). The maximum level of sulfated glycosaminoglycans in the lungs was detected on postinfection day 30 and was related to their involvement in initiation granulomogenesis and development of granulomas. The maximum level of total glycosaminoglycans in mouse serum on postinfection day 90 coincided with minimum level of sulfated glycosaminoglycans in the lungs. This blood/lungs ratio of glycosaminoglycans can be related to the prevalence of low-molecular-weight hyaluronan fragments promoting inflammation and fibrosis in the lungs observed at the end of the experiment (postinfection day 180).

Generalized BCG-induced granulomatous was simulated in BALB/c male mice. The number of tuberculous granulomas in the liver and their size as well as the number of hepatocytes showing vacuolar degeneration increased from day 3 to 180 postinfection. Necrotic changes in hepatocytes were most pronounced at the acute phase of inflammation (days 3 to 30). Proliferative processes in the liver parenchyma in the experimental group were less marked than in the control. Increased content of collagen fibers in the liver was determined by excessive collagen synthesis in necrotic areas as well as increased amount of granulomas and fibroblasts. Enhanced proliferative and fibroplastic activity of fibroblasts in granulomas and liver parenchyma was evidently determined by activated granuloma macrophages. These shifts determined changes in the liver content of hydroxyproline during the acute and chronic periods of the disease.

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