Staphylococcus aureus (S. aureus) is a Gram-positive bacterium that serves as a major pathogen causing bovine mastitis. One of the key intracellular survival mechanisms of S. aureus involves the induction of autophagy. The capacity of S. aureus to subvert autophagy for intracellular survival and replication is strongly linked to its broad array of virulence determinants, which play pivotal roles in infection establishment and immune evasion. One of these virulence factors is phenol-soluble modulin alpha (PSMα), an amphipathic small peptide that plays a key role in the pathogenesis of S. aureus. Utilizing gene-edited S. aureus strain and bovine mammary epithelial cells (BMECs, MAC-T), this study elucidates the involvement of PSMα in autophagy induction during S. aureus infection. The results demonstrated that PSMα knockout attenuated S. aureus-induced autophagy, weakened the activation of the PI3K/Akt/mTOR pathway, and reduced intracellular bacterial load. Our findings elucidate a PSMα-dependent autophagy induction mechanism in S. aureus infection, which is associated with the intracellular survival of S. aureus.
Chen et al. (Thu,) studied this question.
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