Streptococcus agalactiae-induced autophagy of bovine mammary epithelial cell via PI3K/AKT/mTOR pathway
Streptococcus agalactiae (S. agalactiae) infection is a significant cause of mastitis, resulting in loss of cellular homeostasis and tissue damage. Autophagy plays an essential function in cell survival, defense, and the preservation of cellular homeostasis, and is often part of the response to path...
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| Veröffentlicht in: | Journal of dairy research 2022-05, Vol.89 (2), p.178-184 |
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| creator | Qi, Mengzhu Geng, Hao Geng, Na Cui, Yukun Qi, Changxi Cheng, Guodong Song, Kaimin Hu, Liping Liu, Yongxia Liu, Jianzhu Han, Bo |
| description | Streptococcus agalactiae (S. agalactiae) infection is a significant cause of mastitis, resulting in loss of cellular homeostasis and tissue damage. Autophagy plays an essential function in cell survival, defense, and the preservation of cellular homeostasis, and is often part of the response to pathogenic challenge. However, the effect of autophagy induced by S. agalactiae in bovine mammary epithelial cells (bMECs) is mainly unknown. So in this study, an intracellular S. agalactiae infection model was established. Through evaluating the autophagy-related indicators, we observed that after S. agalactiae infection, a significant quantity of LC3-I was converted to LC3-II, p62 was degraded, and levels of Beclin1 and Bcl2 increased significantly in bMECs, indicating that S. agalactiae induced autophagy. The increase in levels of LAMP2 and LysoTracker Deep Red fluorescent spots indicated that lysosomes had participated in the degradation of autophagic contents. After autophagy was activated by rapamycin (Rapa), the amount of p-Akt and p-mTOR decreased significantly, whilst the amount of intracellular S. agalactiae increased significantly. Whereas the autophagy was inhibited by 3-methyladenine (3MA), the number of intracellular pathogens decreased. In conclusion, the results demonstrated that S. agalactiae could induce autophagy through PI3K/Akt/mTOR pathway and utilize autophagy to survive in bMECs. |
| doi_str_mv | 10.1017/S0022029922000243 |
| format | Article |
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Autophagy plays an essential function in cell survival, defense, and the preservation of cellular homeostasis, and is often part of the response to pathogenic challenge. However, the effect of autophagy induced by S. agalactiae in bovine mammary epithelial cells (bMECs) is mainly unknown. So in this study, an intracellular S. agalactiae infection model was established. Through evaluating the autophagy-related indicators, we observed that after S. agalactiae infection, a significant quantity of LC3-I was converted to LC3-II, p62 was degraded, and levels of Beclin1 and Bcl2 increased significantly in bMECs, indicating that S. agalactiae induced autophagy. The increase in levels of LAMP2 and LysoTracker Deep Red fluorescent spots indicated that lysosomes had participated in the degradation of autophagic contents. After autophagy was activated by rapamycin (Rapa), the amount of p-Akt and p-mTOR decreased significantly, whilst the amount of intracellular S. agalactiae increased significantly. Whereas the autophagy was inhibited by 3-methyladenine (3MA), the number of intracellular pathogens decreased. In conclusion, the results demonstrated that S. agalactiae could induce autophagy through PI3K/Akt/mTOR pathway and utilize autophagy to survive in bMECs.</description><identifier>ISSN: 0022-0299</identifier><identifier>EISSN: 1469-7629</identifier><identifier>DOI: 10.1017/S0022029922000243</identifier><identifier>PMID: 35388773</identifier><language>eng</language><publisher>Cambridge, UK: Cambridge University Press</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Autophagy ; Cattle ; Cell survival ; Epithelial cells ; Epithelium ; Fluorescence ; Homeostasis ; Infections ; Intracellular ; Lysosomes ; Mammary gland ; Mastitis ; Rapamycin ; Streptococcus agalactiae ; Streptococcus infections ; TOR protein</subject><ispartof>Journal of dairy research, 2022-05, Vol.89 (2), p.178-184</ispartof><rights>Copyright © The Author(s), 2022. Published by Cambridge University Press on behalf of Hannah Dairy Research Foundation</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c373t-49040de173bf40825b05263f9ce322248bd922c70e8a337605c6a426612671263</citedby><cites>FETCH-LOGICAL-c373t-49040de173bf40825b05263f9ce322248bd922c70e8a337605c6a426612671263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.cambridge.org/core/product/identifier/S0022029922000243/type/journal_article$$EHTML$$P50$$Gcambridge$$H</linktohtml><link.rule.ids>164,314,780,784,27923,27924,55627</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35388773$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qi, Mengzhu</creatorcontrib><creatorcontrib>Geng, Hao</creatorcontrib><creatorcontrib>Geng, Na</creatorcontrib><creatorcontrib>Cui, Yukun</creatorcontrib><creatorcontrib>Qi, Changxi</creatorcontrib><creatorcontrib>Cheng, Guodong</creatorcontrib><creatorcontrib>Song, Kaimin</creatorcontrib><creatorcontrib>Hu, Liping</creatorcontrib><creatorcontrib>Liu, Yongxia</creatorcontrib><creatorcontrib>Liu, Jianzhu</creatorcontrib><creatorcontrib>Han, Bo</creatorcontrib><title>Streptococcus agalactiae-induced autophagy of bovine mammary epithelial cell via PI3K/AKT/mTOR pathway</title><title>Journal of dairy research</title><addtitle>Journal of Dairy Research</addtitle><description>Streptococcus agalactiae (S. agalactiae) infection is a significant cause of mastitis, resulting in loss of cellular homeostasis and tissue damage. Autophagy plays an essential function in cell survival, defense, and the preservation of cellular homeostasis, and is often part of the response to pathogenic challenge. However, the effect of autophagy induced by S. agalactiae in bovine mammary epithelial cells (bMECs) is mainly unknown. So in this study, an intracellular S. agalactiae infection model was established. Through evaluating the autophagy-related indicators, we observed that after S. agalactiae infection, a significant quantity of LC3-I was converted to LC3-II, p62 was degraded, and levels of Beclin1 and Bcl2 increased significantly in bMECs, indicating that S. agalactiae induced autophagy. The increase in levels of LAMP2 and LysoTracker Deep Red fluorescent spots indicated that lysosomes had participated in the degradation of autophagic contents. After autophagy was activated by rapamycin (Rapa), the amount of p-Akt and p-mTOR decreased significantly, whilst the amount of intracellular S. agalactiae increased significantly. Whereas the autophagy was inhibited by 3-methyladenine (3MA), the number of intracellular pathogens decreased. In conclusion, the results demonstrated that S. agalactiae could induce autophagy through PI3K/Akt/mTOR pathway and utilize autophagy to survive in bMECs.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Autophagy</subject><subject>Cattle</subject><subject>Cell survival</subject><subject>Epithelial cells</subject><subject>Epithelium</subject><subject>Fluorescence</subject><subject>Homeostasis</subject><subject>Infections</subject><subject>Intracellular</subject><subject>Lysosomes</subject><subject>Mammary gland</subject><subject>Mastitis</subject><subject>Rapamycin</subject><subject>Streptococcus agalactiae</subject><subject>Streptococcus infections</subject><subject>TOR 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agalactiae-induced autophagy of bovine mammary epithelial cell via PI3K/AKT/mTOR pathway</title><author>Qi, Mengzhu ; Geng, Hao ; Geng, Na ; Cui, Yukun ; Qi, Changxi ; Cheng, Guodong ; Song, Kaimin ; Hu, Liping ; Liu, Yongxia ; Liu, Jianzhu ; Han, Bo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c373t-49040de173bf40825b05263f9ce322248bd922c70e8a337605c6a426612671263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Autophagy</topic><topic>Cattle</topic><topic>Cell survival</topic><topic>Epithelial cells</topic><topic>Epithelium</topic><topic>Fluorescence</topic><topic>Homeostasis</topic><topic>Infections</topic><topic>Intracellular</topic><topic>Lysosomes</topic><topic>Mammary gland</topic><topic>Mastitis</topic><topic>Rapamycin</topic><topic>Streptococcus agalactiae</topic><topic>Streptococcus 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Bo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Streptococcus agalactiae-induced autophagy of bovine mammary epithelial cell via PI3K/AKT/mTOR pathway</atitle><jtitle>Journal of dairy research</jtitle><addtitle>Journal of Dairy Research</addtitle><date>2022-05-01</date><risdate>2022</risdate><volume>89</volume><issue>2</issue><spage>178</spage><epage>184</epage><pages>178-184</pages><issn>0022-0299</issn><eissn>1469-7629</eissn><abstract>Streptococcus agalactiae (S. agalactiae) infection is a significant cause of mastitis, resulting in loss of cellular homeostasis and tissue damage. Autophagy plays an essential function in cell survival, defense, and the preservation of cellular homeostasis, and is often part of the response to pathogenic challenge. However, the effect of autophagy induced by S. agalactiae in bovine mammary epithelial cells (bMECs) is mainly unknown. So in this study, an intracellular S. agalactiae infection model was established. Through evaluating the autophagy-related indicators, we observed that after S. agalactiae infection, a significant quantity of LC3-I was converted to LC3-II, p62 was degraded, and levels of Beclin1 and Bcl2 increased significantly in bMECs, indicating that S. agalactiae induced autophagy. The increase in levels of LAMP2 and LysoTracker Deep Red fluorescent spots indicated that lysosomes had participated in the degradation of autophagic contents. 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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Autophagy Cattle Cell survival Epithelial cells Epithelium Fluorescence Homeostasis Infections Intracellular Lysosomes Mammary gland Mastitis Rapamycin Streptococcus agalactiae Streptococcus infections TOR protein |
| title | Streptococcus agalactiae-induced autophagy of bovine mammary epithelial cell via PI3K/AKT/mTOR pathway |
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