In vitro Study of BCG Granuloma Macrophage Morphofunctional Status

Author:

Shkurupy V.A.12,Arkhipov S.A.12,Akhramenko E.S.1,Solomatina M.V.1,Iljine D.A.1,Neshchadim D.V.1

Affiliation:

1. Research Center of Clinical and Experimental Medicine, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk, Russia

2. Novosibirsk State Medical University, Novosibirsk, Russia

Abstract

We studied the morphofunctional and cytophysiological status of macrophages emigrating from BCG granulomas forming in spleen and free splenic macrophages that are not associated with granulomas. The experimental BCG granulomatosis was induced by intravenous injection of male BALB/c mice with BCG vaccine mycobacteria. The number of granulomas in spleen, their diameter, the proportion of granuloma macrophages with mycobacteria, the number of mycobacteria in granuloma macrophages, the proportion of live bacteria in granuloma macrophages and the number of granulomas macrophages capable of expressing IL-1α, TNF-α, GM-CSF were evaluated. BCG granulomas were explanted in cultures in vitro. Fractions, containing free splenic macrophages from BCG-infected animals, were explanted in separate cultures in vitro. The phagocytic activity of macrophages that migrated from BCG granulomas explanted in cultures one month after mycobacterial infection of mice, was much higher than those of splenic macrophages of intact mice. The phagocytic activity of free macrophages and macrophages from granulomas decreased with time after infection. By contrast, the antimycobacterial activity of free splenic macrophages and macrophages from BCG granulomas increased with time after infection. The correlational analysis showed that there are different correlational relationships between the number of granuloma macrophages expressing IL-1α, TNF-α, GM-CSF and phagocytic activity of macrophages from BCG granulomas. The results of the study are important for understanding the molecular and cellularmechanisms of development of chronic granulomatous inflammation induced by mycobacterial infection.

Publisher

SAGE Publications

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