Staphylococcus aureus induces autophagy in bovine mammary epithelial cells and the formation of autophagosomes facilitates intracellular replication of Staph. Aureus

摘要

Staphylococcus aureus is an important pathogen causingchronic and subclinical mastitis of cows. Autophagyis an important regulatory mechanism that participatesin the elimination of invading pathogenic organisms.Here, we hypothesize that autophagy is involved in theprocess of Staph. aureus survival in bovine mammaryepithelial cells (BMEC). In this study, we detected theexpression of autophagy-related proteins during infectionand assessed the effect of autophagosome formationand degradation on the proliferation of intracellularStaph. aureus. Infection with Staph. aureus increasedthe protein expression of microtubule-associated protein1 light chain 3-II (MAP1LC3, also called LC3-II) andsequestosome-1 (SQSTM1, also called p62) in BMEC.After infection, the formation of the autophagosomesincreased but the autophagosomes and lysosomes couldnot fuse normally to form autolysosomes. When theformation of the autophagosomes was enhanced orthe degradation of the autolysosomes was inhibited,the number of Staph. aureus in the BMEC increased.However, the intracellular proliferation of Staph. aureuswas slowed when formation of autophagosomes wasinhibited. Therefore, autophagy was induced in BMECchallenged by Staph. aureus but the autophagic fluxwas obstructed. Inhibiting the formation of autophagosomesin BMEC facilitated the clearance of intracellularStaph. aureus, which may offer a new strategy forthe treatment of mastitis in cows.