The Monocyte in Tuberculosis

The interaction between Mycobacterium tuberculosis and monocytes/macrophages in the early phase of infection is crucial for the pathogenesis of the disease. Pathogens have developed specific mechanisms that allow them to estabUsh a close interaction with host cells and to escape immune response (Ameisen et al. 1994). 

Employing immunocytochemical methods, Buchwalow et al. (1997) provided evidence that a-subunits of stimulatory and inhibitory G-proteins and protein kinase C-P as well as two major cyto-skeletal components, microfilaments and microtubules, participated in uptake of Mycobacterium bo-vis BCG by human macrophages and co-localized in phagosomes. 

Macrophages that are unable to kill intracellu-larly replicating mycobacteria allow their multiplication until the cell bursts. In the first stage of tuberculosis necrosis is the cellular event responsible for macrophage death (Dannenberg jr. and Toma-SHEFSKI 1988). 

The a-subunit of the clotting factor XIII (FXIIIa) has been shown in tuberculous infections as well as in sarcoidosis to be synthesised by macrophages identified by immunohistochemistry predominantly in the periphery of granulomas, whereas the centres were generally devoid of these cells (Probst-Cousin et al. 1997). 

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