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Intracellular Staphylococcus aureus inhibits autophagy of bovine mammary epithelial cells through activating p38α

Published online by Cambridge University Press:  24 August 2021

Run Wang
Affiliation:
College of Veterinary Medicine, Shandong Agricultural University, Tai'an, Shandong, China
Wen Zhang
Affiliation:
College of Veterinary Medicine, Shandong Agricultural University, Tai'an, Shandong, China
Lumei Wang
Affiliation:
College of Veterinary Medicine, Shandong Agricultural University, Tai'an, Shandong, China
Na Geng
Affiliation:
College of Veterinary Medicine, Shandong Agricultural University, Tai'an, Shandong, China
Xiaozhou Wang
Affiliation:
College of Veterinary Medicine, Shandong Agricultural University, Tai'an, Shandong, China
Meihua Zhang
Affiliation:
College of Veterinary Medicine, Shandong Agricultural University, Tai'an, Shandong, China
Jianzhu Liu*
Affiliation:
Research Center for Animal Disease Control Engineering, Shandong Agricultural University, Tai'an, Shandong, China
Yongxia Liu*
Affiliation:
College of Veterinary Medicine, Shandong Agricultural University, Tai'an, Shandong, China
Bo Han
Affiliation:
College of Veterinary Medicine, China Agricultural University, Beijing, China
*
Author for correspondence: Yongxia Liu, Email: [email protected]; Jianzhu Liu, Email: [email protected]
Author for correspondence: Yongxia Liu, Email: [email protected]; Jianzhu Liu, Email: [email protected]

Abstract

Staphylococcus aureus is a common pathogen of bovine mastitis which can induce autophagy and inhibit autophagy flux, resulting in intracellular survival and persistent infection. The aim of the current study was to investigate the role of p38α in the autophagy induced by intracellular S. aureus in bovine mammary epithelial cells. An intracellular infection model of MAC-T cells was constructed, and activation of p38α was examined after S. aureus invasion. Through activating/inhibiting p38α by anisomycin/SB203580, the autophagosomes, LC3 and p62 level were analyzed by immunofluorescence and western blot. To further study the detailed mechanism of p38α, phosphorylation of ULK1ser757 was also detected. The results showed that intracellular S. aureus activated p38α, and the activation developed in a time-dependent manner. Inhibition of p38α promoted intracellular S. aureus-induced autophagy flow, up-regulated the ratio of LC3 II/I, reduced the level of p62 and inhibited the phosphorylation of ULK1ser757, whereas the above results were reversed after activation of p38α. The current study indicated that intracellular S. aureus can inhibit autophagy flow by activating p38α in bovine mammary epithelial cells.

Type
Research Article
Copyright
Copyright © The Author(s), 2021. Published by Cambridge University Press on behalf of Hannah Dairy Research Foundation

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Footnotes

*

These authors contributed equally to this work.

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