Endogenous nitric oxide promotes <i>Staphylococcus aureus</i> virulence by activating autophagy.

ABSTRACT: Endogenous nitric oxide (NO) is a small molecule that has been demonstrated to affect the physiology and survival of bacteria. The role of endogenous NO for Staphylococcus aureus survival inside host cells remains unclear. Here, we show that the production of endogenous NO by bacterial nitrate reductase (NR) is affected by molybdopterin biosynthesis protein A (MoeA), which is essential for molybdenum cofactor synthesis in S. aureus. During the infection, the production of endogenous NO promotes S. aureus survival inside macrophages by initiating cellular autophagy. Mechanistically, bacterial endogenous NO can modify the host regulatory protein thioredoxin vis S-nitrosylation, subsequently triggering the phosphorylation of the JNK-Bcl-2 pathway and promoting the initiat

SUBMITTER: Nurxat N 

PROVIDER: S-EPMC11980563 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature