Mechanism of intracellular persistence of Staphylococcus aureus by novel function of toxic shock syndrome toxin-1

研究了中毒性休克综合征毒素-1（TSST-1）对金黄色葡萄球菌感染上皮细胞的影响。TSST-1不改变对上皮细胞HeLa 229、HEK 293和407的粘附和侵袭。然而，TSST-1减少了自噬体在营养饥饿细胞或雷帕霉素处理的细胞中的积累，表明TSST-1抑制自噬。此外，这种抑制不需要超抗原活性，可能参与自噬体形成过程，而不是自噬体降解。从感染后第5天开始，产TSST-1的S.与非生产菌株相比，金黄色葡萄球菌的存活率下降，表明TSST-1可能促进金黄色葡萄球菌的细胞内持续存在。金黄色葡萄球菌在上皮细胞。

Effect of toxic shock syndrome toxin-1 (TSST-1) on Staphylococcus aureus infection in the epithelial cells was investigated. TSST-1 did not alter the adhesion and invasion into the epithelial cells, HeLa 229, HEK293 and 407. However, TSST-1 reduced the accumulation of autophagosomes in nutrient starved cells or rapamycin-treated cells, suggesting that TSST-1 suppresses autophagy. In addition, this suppression did not require superantigenic activity and might be involved in the autophagosome formation process rather than autophagosome degradation. From day 5 after infection, intracellular bacterial number and cytotoxicity of TSST-1-producing S. aureus were deceased in comparison to non-producing strain, suggesting that TSST-1 may promote intracellular persistence of S. aureus in the epithelial cells.