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Staphylococcus aureus Bacteriophage Suppresses LPS-Induced Inflammation in MAC-T Bovine Mammary Epithelial Cells

机译:金黄色葡萄球菌噬菌体可抑制LPS诱导的MAC-T牛乳腺上皮细胞炎症

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摘要

Several previous studies have shown that bacteriophages can significantly affect the production of various cytokines. The aim of this present study was to investigate the inflammatory effects and mechanisms of bacteriophage vB_SauM_JS25 in stimulated MAC-T bovine mammary epithelial cells by real-time polymerase chain reaction (PCR) and Western blotting. Experiments show that vB_SauM_JS25 reduces Staphylococcus aureus- or lipopolysaccharide (LPS)-induced levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, IL-8, IL-10, and regulated on activation, normal T cell expressed and secreted (RANTES) mRNA in MAC-T cells, in a manner expected to be unrelated to its antibacterial action. Moreover, S. aureus bacteriophage vB_SauM_JS25 suppressed the LPS-induced phosphorylation of nuclear factor (NF)-κB p65, which may represent an important mechanism mediating these effects. A carefully regulated balance between activation and inhibition by bacteriophages must be kept avoiding inappropriate inflammatory responses. The ability of vB_SauM_JS25 to influence the immune response highlights the potential development and application of bacteriophage-based therapies and may represent a novel anti-inflammatory therapeutic strategy.
机译:先前的一些研究表明,噬菌体可以显着影响各种细胞因子的产生。本研究的目的是通过实时聚合酶链反应(PCR)和Western印迹研究噬菌体vB_SauM_JS25在刺激的MAC-T牛乳腺上皮细胞中的炎症作用和机制。实验表明,vB_SauM_JS25可降低金黄色葡萄球菌或脂多糖(LPS)诱导的肿瘤坏死因子-α(TNF-α),白介素(IL)-1β,IL-6,IL-8,IL-10的水平,并对其进行调节激活,正常T细胞在MAC-T细胞中表达和分泌(RANTES)mRNA,其方式与其抗菌作用无关。此外,金黄色葡萄球菌噬菌体vB_SauM_JS25抑制LPS诱导的核因子(NF)-κBp65磷酸化,这可能是介导这些作用的重要机制。必须保持噬菌体在激活和抑制之间的仔细调节平衡,以避免不适当的炎症反应。 vB_SauM_JS25影响免疫反应的能力突显了基于噬菌体的疗法的潜在发展和应用,可能代表了一种新型的抗炎治疗策略。

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