南美超级胎牛血清999尝鲜特惠
金黄色葡萄球菌β-溶血素通过破坏褶皱形成机制，削弱巨噬细胞的吞噬功能。
Staphylococcus aureus β-hemolysin impairs macrophage phagocytosis by disrupting ruffle formation
Li Qi, Chen Nan, Sun Yu, Li Jingjing, Liu Chenghua, Yang Guang
Journal：BMC MICROBIOLOGY
IF：5.4
DOI：10.1186/s12866-026-05557-9
PMID：
Published：2026-08-24
research field：免疫学微生物学宿主-病原体相互作用细菌致病机制细胞微生物学
Abstract
Staphylococcus aureus , a major human pathogen, evades host immunity via multiple virulence factors. Macrophage phagocytosis is critical for clearing S. aureus to protect against infection. In this study, we demonstrated that β-hemolysin (Hlb), a sphingomyelinase (SMase), significantly impaired the phagocytic capacity of macrophages, which was strictly dependent on its SMase activity. Mechanistically, Hlb treatment significantly disrupted the formation of F-actin-rich membrane ruffles, a critical step in phagocytic uptake. Further in vivo study demonstrated that the presence of Hlb markedly increased bacterial burden. Collectively, these findings identify Hlb as a key virulence factor that subverts macrophage protection by disrupting membrane ruffle formation, thereby enhancing S. aureus survival during infection.
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