We therefore propose a novel molecular mechanism by which BH inhibits Salmonella-induced gastroenteritis via the T3SS (Figure 7): under normal infection conditions, S. Typhimurium injects effector proteins through its T3SS to suppress the expression of SIRT1/AMPK, weakening the original inhibition of mTOR and thus reducing autophagosome formation; this prevents lysosomes from degrading bacteria, allowing the bacteria to survive intracellularly. Here, MTOR is linked to gastroenteritis.