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Melatonin Maintains Homeostasis and Potentiates the Anti-inflammatory Response in Staphylococcus aureus-Induced Mastitis through microRNA-16b/YAP1
Journal of Agricultural and Food Chemistry ( IF 6.1 ) Pub Date : 2022-11-18 , DOI: 10.1021/acs.jafc.2c05904
Zhi Chen 1 , Kun Wang 1 , Jiahe Guo 1 , Jingpeng Zhou 1 , Juan J Loor 2 , Zhangping Yang 1 , Yi Yang 1
Affiliation  

Staphylococcus aureus is a highly infectious pathogen and is a considerable threat to food hygiene and safety. Although melatonin is thought to exert an ameliorative effect on bovine mastitis, the regulatory mechanisms are unclear. In this study, we first verified the therapeutic effect of melatonin against S. aureus in vitro and in vivo, a screening of differentially expressed miRNAs and mRNAs among the blank, and S. aureus and melatonin + S. aureus groups by high-throughput sequencing identified miR-16b and YAP1, which exhibited 1.95-fold upregulated and 1.05-fold downregulated expression, respectively. Moreover, epigenetic studies showed that S. aureus inhibited miR-16b expression by methylation (increased DNMT1 expression). Additionally, the DNMT1 expression level was significantly decreased by melatonin treatment, which might indicate that the inhibition of DNMT1 by melatonin reduces the effect of S. aureus on miR-16b. The flow cytometry, scanning and transmission electron microscopy, EdU assay, and cell morphology results indicated that miR-16b in bovine mammary epithelial cells (in vitro) and in mice (in vivo) can modulate the maintenance of homeostasis and potentiate the anti-inflammatory response. In addition, YAP1 was demonstrated to be the target gene of miR-16b through quantitative real-time polymerase chain reaction, western blot, RNA immunoprecipitation, and functional assays. This study indicates that melatonin inhibits S. aureus-induced inflammation via microRNA-16b/YAP1-mediated regulation, and these findings might provide a new strategy for the prevention of bovine mastitis, facilitating further studies good of zoonotic diseases caused by S. aureus infection.

中文翻译:

褪黑激素通过 microRNA-16b/YAP1 维持稳态并增强金黄色葡萄球菌诱导的乳腺炎的抗炎反应

金黄色葡萄球菌是一种传染性很强的病原体,对食品卫生和安全构成相当大的威胁。虽然褪黑激素被认为对牛乳腺炎有改善作用,但调节机制尚不清楚。本研究首先通过高通量测序验证了褪黑素对金黄色葡萄球菌的体外和体内治疗作用,筛选了空白、金黄色葡萄球菌和褪黑素+金黄色葡萄球菌组中差异表达的miRNAs和mRNAs鉴定了 miR-16b 和YAP1,它们分别表现出 1.95 倍的上调和 1.05 倍的下调表达。此外,表观遗传学研究表明金黄色葡萄球菌通过甲基化抑制 miR-16b 表达(增加 DNMT1 表达)。此外,褪黑激素处理显着降低了DNMT1表达水平,这可能表明褪黑激素对DNMT1的抑制降低了金黄色葡萄球菌对 miR-16b 的影响。流式细胞术、扫描和透射电子显微镜、EdU 测定和细胞形态学结果表明,miR-16b 在牛乳腺上皮细胞(体外)和小鼠(体内)中可以调节体内平衡的维持并增强抗炎作用。回复。此外,YAP1通过定量实时聚合酶链反应、蛋白质印迹、RNA 免疫沉淀和功能测定证明是 miR-16b 的靶基因。本研究表明褪黑激素通过microRNA-16b/ YAP1介导的调节抑制金黄色葡萄球菌引起的炎症,这些发现可能为牛乳腺炎的预防提供新的策略,促进金黄色葡萄球菌感染引起的人畜共患疾病的进一步研究.
更新日期:2022-11-18
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