Modulation of macrophage antimicrobial mechanisms by pathogenic mycobacteria.

Tuberculosis remained a mysterious disease until Koch was able to demonstrate in the late 1800s that it was caused by a bacterium spread by aerosols, Mycobacterium tuberculosis. Today, tuberculosis still is a major health problem causing approximately 2 million deaths annually with about one third of the world's population being latently infected with M. tuberculosis. The secret of success for M. tuberculosis lies in its ability to persist inside host cells, the macrophages. Whereas macrophages are designed to destroy any incoming microbe, pathogenic mycobacteria have evolved strategies to survive within macrophages by preventing phagosome-lysosome fusion, thereby creating a niche that allows them to persist within an otherwise hostile environment. In this contribution, we discuss recent advances in our understanding of the interplay between the host and this pathogen that lead to survival of mycobacteria within macrophages.