Mycobacterium tuberculosis (Mtb) uses alveolar macrophages as primary host cells during
infection. In response to an infection, macrophages switch from pyruvate oxidation to …

In order to mount an appropriate immune response to infection, the macrophage must alter
its metabolism by increasing aerobic glycolysis and concomitantly decreasing oxidative …

Mycobacterium tuberculosis (Mtb) is thought to preferentially rely on fatty acid metabolism to
both establish and maintain chronic infections. Its metabolic network, however, allows …

Infection with Mycobacterium tuberculosis (Mtb) leading to tuberculosis (TB) disease
continues to be a major global health challenge. Critical barriers, including but not limited to …

Mycobacterium tuberculosis (Mtb) adapts to persist in a nutritionally limited macrophage
compartment. Lipoamide dehydrogenase (Lpd), the third enzyme (E3) in Mtb's pyruvate …

Mycobacterium tuberculosis (Mtb) persists for prolonged periods in macrophages, where it
must adapt to metabolic limitations and oxidative/nitrosative stress. However, little is known …

Mycobacterium tuberculosis (Mtb) has adapted its metabolism for persistence in the human
macrophage. The adaptations are likely to involve Mtb's core intermediary metabolism …

Mycobacterium tuberculosis (Mtb) displays a high degree of metabolic plasticity to adapt to
challenging host environments. Genetic evidence suggests that Mtb relies mainly on fatty …

Metabolic adaptation to the host niche is a defining feature of the pathogenicity of
Mycobacterium tuberculosis (Mtb). In vitro, Mtb is able to grow on a variety of carbon …

Bacterial nutrition is an essential aspect of host–pathogen interaction. For the intracellular
pathogen Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis in humans …