Abstract
Species of the genus Mycobacterium are capable of inducing cell apoptosis. Infected cells with M. tuberculosis undergo apoptosis through a caspase-dependent pathway. We have previously shown that whole Mycobacterium bovis cells and derived crude protein extracts were able to trigger apoptosis through a caspase independent mechanism. However, the identity of the protein or protein fractions capable of inducing apoptosis has not been determined. In this study, bovine macrophages were incubated in the presence of Mycobacterium tuberculosis recombinant proteins and Mycobacterium bovis protein extracts to identify proteins capable of inducing apoptosis. A subgroup of proteins and protein extracts from strains of the Mycobacterium tuberculosis complex were shown to induce DNA fragmentation in bovine macrophages through a caspase independent pathway. Our findings suggest that bovine macrophages may elicit a different response to mycobacterium infection than that displayed by murine or human cells.
Highlights
Tuberculosis is responsible for the deaths of millions of people each year and is the second leading cause of death due to an infectious disease after the human immunodeficiency virus (HIV)
The main goal of this study was to assess the effect of Mycobacterium tuberculosis recombinant proteins, and of Mycobacterium bovis derived protein extracts on apoptosis induction in bovine macrophages
Figure 1. 12% SDS PAGE stained with Coomassie R-250 blue, showing bands from a soluble protein extract (SE) and culture filtrate protein extract (CFE) derived from a M. bovis AN5 culture
Summary
Tuberculosis is responsible for the deaths of millions of people each year and is the second leading cause of death due to an infectious disease after the human immunodeficiency virus (HIV). Pathogenesis of mycobacteria relates to their ability to survive inside host cells, especially in immune cells such as macrophages and monocytes.[3] mycobacteria can disrupt the activation and phagocytic processes of immune cells.[4] Species from the M. tuberculosis complex (MTC) can, for instance, survive in macrophages by inhibiting acidification of the phagosomal compartment thereby preventing the phagosome-lysosome fusion; adapting to the intracellular environment of the macrophage, but turning it into their replication niche.[5]
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