Phagosomal rupture by Mycobacterium tuberculosis results in toxicity and host cell death.

ABSTRACT: Survival within macrophages is a central feature of Mycobacterium tuberculosis pathogenesis. Despite significant advances in identifying new immunological parameters associated with mycobacterial disease, some basic questions on the intracellular fate of the causative agent of human tuberculosis in antigen-presenting cells are still under debate. To get novel insights into this matter, we used a single-cell fluorescence resonance energy transfer (FRET)-based method to investigate the potential cytosolic access of M. tuberculosis and the resulting cellular consequences in an unbiased, quantitative way. Analysis of thousands of THP-1 macrophages infected with selected wild-type or mutant strains of the M. tuberculosis complex unambiguously showed that M. tuberculosis induced a change in the

SUBMITTER: Simeone R 

PROVIDER: S-EPMC3271072 | biostudies-literature | 2012 Feb

REPOSITORIES: biostudies-literature