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Mycobacterium tuberculosis virulence correlates with mitochondrial cytochrome c release in infected macrophages
E Abarca-Rojano1, P Rosas-Medina, P Zamudio-Cortéz
1Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, México D.F., México.
Abstract:
Mitochondria are at the centre of molecular events involved in energy production, cell survival and apoptosis. Mitochondrial membrane potential (Deltapsim) is maintained by cellular catabolic reactions and the electron transport chain of which cytochrome c is a constituent, whereas the proton leak pathway, ATP synthesis and turnover consume it. Mitochondrial alterations such as a drop in Deltapsim, swelling and cytochrome c release have been observed in apoptosis. However, there is a paucity of information concerning mitochondrial function in the course of intracellular infections, a process that must certainly induce stress on the host cell. This work analyses the effect that two strains of mycobacteria of opposing virulence have on the mitochondria of murine macrophages in the early stages of infection. It was found that infection of J774 cells with both Mycobacterium tuberculosis H37Ra and M. tuberculosis H37Rv readily induced changes in Deltapsim as well as in mitochondrial morphology at the ultrastructural level. In addition, an increase in cytosolic ATP was found at 24 h post infection with both strains of M. tuberculosis. Interestingly, only M. tuberculosis H37Rv was able to induce cytochrome c release from mitochondria to the cytosol, thus suggesting the occurrence in M. tuberculosis H37Rv of a specific factor(s) capable of regulating cytochrome c translocation. The precise role of cytochrome c release in the context of a mycobacterial infection remains to be elucidated.
Insights
Mycobacterium tuberculosis infection alters mitochondrial membrane potential and morphology in macrophages. Virulent M. tuberculosis H37Rv, but not H37Ra, also causes cytochrome c release, suggesting a specific virulence factor.
Area of Science:
- Cellular Biology
- Mitochondrial Biology
- Infectious Disease Immunology
Background:
- Mitochondria are crucial for cellular energy production, survival, and apoptosis.
- Mitochondrial membrane potential (ΔΨm) and morphology are key indicators of cellular health.
- Information on mitochondrial function during intracellular infections, particularly mycobacterial infections, is limited.
Purpose of the Study:
- To investigate the impact of two Mycobacterium tuberculosis strains with differing virulence on murine macrophage mitochondria during early infection stages.
- To analyze changes in mitochondrial membrane potential, morphology, and key molecular players like cytochrome c.
Main Methods:
- Infection of J774 murine macrophage cell line with Mycobacterium tuberculosis H37Ra and M. tuberculosis H37Rv.
- Assessment of mitochondrial membrane potential (ΔΨm) and ultrastructural morphology.
- Measurement of cytosolic ATP levels and cytochrome c release.
Main Results:
- Both M. tuberculosis strains induced alterations in ΔΨm and mitochondrial morphology.
- Cytosolic ATP levels increased at 24 hours post-infection with both strains.
- Only the virulent M. tuberculosis H37Rv strain induced cytochrome c release into the cytosol.
Conclusions:
- Mycobacterium tuberculosis infection significantly impacts macrophage mitochondrial integrity and function.
- Virulent M. tuberculosis H37Rv possesses a factor that promotes cytochrome c release, potentially influencing host cell fate.
- The exact role of cytochrome c release in mycobacterial pathogenesis requires further investigation.
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