Mycobacterium tuberculosis, the bacterium that causes tuberculosis (TB), mainly grows within host cells. Lerner et al. studied the lifestyle of M. tuberculosis within human macrophages by inspecting them with a combination of live-cell imaging, correlative light and electron microscopy, and single-cell analysis. After infection, some of the macrophages became necrotic and had damaged plasma membranes, although they still supported mycobacterial proliferation. Indeed, inhibiting necrosis compromised the macrophages' ability to support mycobacterium replication. Eventually, such cells ruptured to release progeny mycobacteria to infect new host cells. The ability of this microbe to exploit necrotic macrophages as a nutrient-rich haven isolated from host defenses likely contributes to its success in resisting antimycobacterial therapies.
J. Cell Biol. 216, 583 (2017).