Streptococcus lutetiensis Induces Autophagy via Oxidative Stress in Bovine Mammary Epithelial Cells

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dc.contributor.authorChen, Peng
dc.contributor.authorYang, Jingyue
dc.contributor.authorWu, Naiwen
dc.contributor.authorHan, Bo
dc.contributor.authorKastelic, John P.
dc.contributor.authorGao, Jian
dc.date.accessioned2022-02-13T08:00:23Z
dc.date.available2022-02-13T08:00:23Z
dc.date.issued2022-02-07
dc.date.updated2022-02-13T08:00:22Z
dc.description.abstractStreptococcus lutetiensis, an emerging pathogen causing bovine mastitis, has not been well characterized. We reported that S. lutetiensis was pathogenic both in vivo and in vitro and caused inflammatory reactions in the mammary gland. However, roles of autophagy and oxidative stress in the pathogenesis of S. lutetiensis-induced mastitis are unclear. In this study, an autophagy model of S. lutetiensis-infected bovine mammary epithelial cells (bMECs) was used to assess oxidative stress and autophagy flux. Expressions of Beclin1, light chain 3II, and Sequestosome 1/p62 were elevated in bMECs after S. lutetiensis infection. In addition, autophagosome and lysosome formation confirmed autophagy occurred. Based on LysoTracker Red and acridine orange, lysosome degradation was blocked, and lower expressions of lysosomal-associated membrane protein 2, cathepsins D, and cathepsins L confirmed lysosomal damage. Concurrently, the nuclear factor erythroid 2-related factor 2 (Nrf2), kelch-like ECH-associated protein 1 (Keap1), heme oxygenase 1 (HO1), and NAD (P)H: quinone oxidoreductase 1 (NQO1), and basilic proteins associated with the Nrf2/Keap1 signaling pathway, were detected. Decreased keap1 and increased Nrf2, HO1, NQO1, and reactive oxygen species (ROS) indicated increased oxidative stress. Treatment with N-Acetyl-L-cysteine (NAC), an ROS inhibitor, decreased both oxidative stress and autophagy. Therefore, we concluded that S. lutetiensis caused intracellular oxidative stress and autophagy in bMECs. In addition, crosstalk between autophagy and oxidative stress affected the autophagic flux and blocked downstream autophagy. The Nrf2-keap1-p62 pathway participated in this process, with ROS acting upstream of these effects, interfering with normal cell functions.
dc.description.versionPeer Reviewed
dc.identifier.citationPeng Chen, Jingyue Yang, Naiwen Wu, Bo Han, John P. Kastelic, and Jian Gao, “Streptococcus lutetiensis Induces Autophagy via Oxidative Stress in Bovine Mammary Epithelial Cells,” Oxidative Medicine and Cellular Longevity, vol. 2022, Article ID 2549772, 16 pages, 2022. doi:10.1155/2022/2549772
dc.identifier.urihttp://dx.doi.org/10.1155/2022/2549772
dc.identifier.urihttp://hdl.handle.net/1880/114412
dc.identifier.urihttps://dx.doi.org/10.11575/PRISM/39603
dc.language.rfc3066en
dc.rights.holderCopyright © 2022 Peng Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
dc.titleStreptococcus lutetiensis Induces Autophagy via Oxidative Stress in Bovine Mammary Epithelial Cells
dc.typeJournal Article
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