Fig. 7: STM modulates macrophage glucose metabolism to support efficient intracellular replication and systemic infection.

STM translocates the effector SopE2 through the SPI-1 type III secretion system (T3SS), which represses macrophage serine synthesis and leads to the accumulation of glycolytic intermediates in macrophages. The decreased glucose level in macrophages induces the import of macrophage-derived 3PG as a main carbon source in order to support growth via VrpA in STM and senses increased pyruvate or lactate levels in macrophages to activate SPI-2 T3SS expression, thus promoting its intracellular replication and systemic infection.