Intracellular Staphylococcus aureus Infection Decreases Milk Protein Synthesis by Preventing Amino Acid Uptake in Bovine Mammary Epithelial Cells.
Intracellular Staphylococcus aureus Infection Decreases Milk Protein Synthesis by Preventing Amino Acid Uptake in Bovine Mammary Epithelial Cells.
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DOI：
10.3389/fvets.2021.756375
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发表时间：
2021
影响因子：
3.2
通讯作者：
Wang Z
中科院分区：
文献类型：
--
作者：
Chen Y;Ma Y;Ji Q;Yang X;Feng X;Yao R;Cheng X;Li T;Wang Y;Wang Z
金黄色葡萄球菌(S.金黄色葡萄球菌）是奶牛乳房炎的主要病原体之一，其在乳房组织中定居并内化到乳房上皮细胞中，引起乳房的细胞内感染。患有由链球菌引起的乳腺炎的奶牛所产的奶。金黄色葡萄球菌与产量降低和蛋白质组成变化有关。然而，关于诱导乳腺炎的细菌如何影响原料乳的信息有限，特别是关于蛋白质含量和蛋白质组成的信息。本研究的主要目的是探讨S.金黄色葡萄球菌感染影响牛乳腺上皮细胞（BMEC）中乳蛋白的合成。BMEC感染S.金黄色葡萄球菌（S. aureus）感染后，用ELISA法测定乳蛋白和氨基酸含量。金黄色葡萄球菌侵入。Western blot、免疫荧光和RT-qPCR检测mTORC1信号通路、转录因子NF-κ B和STAT5的活性以及氨基酸转运蛋白SLC1A3和SLC7A5的表达。S.金黄色葡萄球菌在体外被BMEC内化，内化细菌在细胞内增殖。在S.金黄色葡萄球菌侵染后，乳蛋白表达下调，BMEC从培养基中吸收Glu、Asp、Leu的水平下降，外源氨基酸诱导的β-酪蛋白合成水平下降。此外，mTORC1信号传导、NF-κ B和STAT5的活性受损，SLC1A3和SLC7A5下调。100 nM雷帕霉素处理8小时可抑制BMEC中NF-κ B和STAT5活性、SLC1A3和SLC7A5表达以及乳蛋白合成。因此，mTORC1通过NF-κ B和STAT5调节SLC1A3和SLC7A5的表达。这些发现构成了S.金黄色葡萄球菌感染通过减少BMEC中氨基酸的摄取来抑制乳蛋白的合成。
Staphylococcus aureus (S. aureus) is one of the main pathogens in cow mastitis, colonizing mammary tissues and being internalized into mammary epithelial cells, causing intracellular infection in the udder. Milk that is produced by cows that suffer from mastitis due to S. aureus is associated with decreased production and changes in protein composition. However, there is limited information on how mastitis-inducing bacteria affect raw milk, particularly with regard to protein content and protein composition. The main purpose of this work was to examine how S. aureus infection affects milk protein synthesis in bovine mammary epithelial cells (BMECs). BMECs were infected with S. aureus, and milk protein and amino acid levels were determined by ELISA after S. aureus invasion. The activity of mTORC1 signaling and the transcription factors NF-κB and STAT5 and the expression of the amino acid transporters SLC1A3 and SLC7A5 were measured by western blot or immunofluorescence and RT-qPCR. S. aureus was internalized by BMECs in vitro, and the internalized bacteria underwent intracellular proliferation. Eight hours after S. aureus invasion, milk proteins were downregulated, and the level of BMECs that absorbed Glu, Asp, and Leu from the culture medium and the exogenous amino acids induced β-casein synthesis declined. Further, the activity of mTORC1 signaling, NF-κB, and STAT5 was impaired, and SLC1A3 and SLC7A5 were downregulated. Eight hours of treatment with 100 nM rapamycin inhibited NF-κB and STAT5 activity, SLC1A3 and SLC7A5 expression, and milk protein synthesis in BMECs. Thus mTORC1 regulates the expression of SLC1A3 and SLC7A5 through NF-κB and STAT5. These findings constitute a model by which S. aureus infection suppresses milk protein synthesis by decreasing amino acids uptake in BMECs.
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影响因子：
64.5
作者：
Demetriades C;Doumpas N;Teleman AA
通讯作者：
Teleman AA
影响因子：
4.8
作者：
Karki, Pratap;Kim, Clifford;Lee, Eunsook
通讯作者：
Lee, Eunsook
影响因子：
3.5
作者：
Aryana, Kayanush J.;Olson, Douglas W.
通讯作者：
Olson, Douglas W.
影响因子：
2.1
作者：
Akerstedt, Maria;Wredle, Ewa;Johansson, Monika
通讯作者：
Johansson, Monika
影响因子：
2.1
作者：
Kayano, Mitsunori;Itoh, Megumi;Grohn, Yrjo T.
通讯作者：
Grohn, Yrjo T.