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Updated: Jan 8, 2026

Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
Published on: January 17, 2025
Staphylococcus aureus escapes endosomes and autophagosomes via α-hemolysin
Huiling Xu1, Changxi Qi1, Chaonan Qu1
1College of Veterinary Medicine, Shandong Agricultural University, Tai'an, Shandong 271018, China.
None:
The interplay between endosomal and autophagic pathways is crucial for intracellular transport and modulation of pathogen replication. However, the mechanisms underlying the interaction between endosomes and autophagosomes (APs) in the context of Staphylococcus aureus (S. aureus) infection are not well understood. Specifically, the fusion of multivesicular bodies (MVBs) or recycled endosomes (REs) with APs remains unexplored. Here, we reveal that S. aureus induces crosstalk between endosomes and APs, a process modulated by Ca2+ influx. Depletion of Rab11A from REs impairs APs formation and trafficking. Meanwhile, we identify α-hemolysin (α-toxin, Hla) as a key virulence factor in S. aureus-induced membrane damage. α-Hemolysin facilitates S. aureus escape from vesicles, contributing to cytotoxicity and membrane disruption.
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