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Human-origin Lactobacillus salivarius AR809 protects against immunosuppression in S. aureus-induced pharyngitis via Akt-mediated NF-κB and autophagy signaling pathways.
Food & Function ( IF 5.1 ) Pub Date : 2020-01-20 , DOI: 10.1039/c9fo02476j Guochao Jia 1 , Xiaofeng Liu , Na Che , Yongjun Xia , Guangqiang Wang , Zhiqiang Xiong , Hui Zhang , Lianzhong Ai
Food & Function ( IF 5.1 ) Pub Date : 2020-01-20 , DOI: 10.1039/c9fo02476j Guochao Jia 1 , Xiaofeng Liu , Na Che , Yongjun Xia , Guangqiang Wang , Zhiqiang Xiong , Hui Zhang , Lianzhong Ai
Affiliation
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Lactobacillus salivarius AR809 is a newly discovered probiotic strain from a healthy human pharynx and has potential ability to adhere to the pharyngeal epithelium and inhibit Staphylococcus aureus (S. aureus)-induced inflammatory response. Pharyngeal spray administration of AR809 exhibited protective effects in a S. aureus-induced mouse model of pharyngitis. The inhibitory effect and underlying molecular mechanism of AR809 on S. aureus-stimulated pharyngitis were further investigated. AR809 significantly increased phagocytosis and bactericidal activity, reduced the production of inflammatory mediators (intracellular reactive oxygen species (ROS), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), nitric oxide (NO), inducible NOS (iNOS)) and the expression of inflammatory cytokines (tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β)), and induced macrophages to adopt the M2 phenotype. AR809 also attenuated S. aureus-induced phosphorylations of protein kinase B (Akt) and rapamycin (mTOR), and elevated the autophagic protein (light chain 3 from II (LC3-II) and Beclin-1) level. Furthermore, AR809 inhibited nuclear transcription factor kappa-B (NF-κB) activation by suppressing the nuclear translocation of NF-κB p65. Likewise, 740Y-P (a PI3K activator) decreased the anti-inflammatory effect of AR809 against S. aureus-induced inflammatory response, while AR809 treatments with wortmannin (a PI3K inhibitor) markedly reversed this inflammatory response. AR809 prevents S. aureus-induced pharyngeal inflammatory response, possibly by regulating TLR/PI3K/Akt/mTOR signalling pathway-related autophagy and TLR/PI3K/Akt/IκB/NF-κB pathway activity, and therefore has potential for use in preventing pharyngitis and other inflammatory diseases.
中文翻译：
人源唾液乳杆菌AR809可通过Akt介导的NF-κB和自噬信号通路防止金黄色葡萄球菌诱导的咽炎中的免疫抑制。
唾液乳杆菌AR809是一种新发现的益生菌菌株，来自健康的人类咽部，具有潜在的粘附咽上皮和抑制金黄色葡萄球菌（S. aureus）诱导的炎症反应的能力。喷洒AR809的咽部喷雾剂在金黄色葡萄球菌诱导的咽炎小鼠模型中显示出保护作用。进一步研究了AR809对金黄色葡萄球菌刺激的咽炎的抑制作用及其潜在的分子机制。AR809显着增加了吞噬作用和杀菌活性，减少了炎症介质的产生（细胞内活性氧（ROS），前列腺素E2（PGE2），环氧合酶2（COX-2），一氧化氮（NO），诱导型NOS（iNOS））和炎性细胞因子（肿瘤坏死因子-α（TNF-α）和白介素-1β（IL-1β））的表达，并诱导巨噬细胞采用M2表型。AR809还减弱了金黄色葡萄球菌诱导的蛋白激酶B（Akt）和雷帕霉素（mTOR）的磷酸化，并提高了自噬蛋白（II轻链3（LC3-II）和Beclin-1）的水平。此外，AR809通过抑制NF-κBp65的核转运来抑制核转录因子kappa-B（NF-κB）活化。同样，740Y-P（PI3K激活剂）降低了AR809对金黄色葡萄球菌诱导的炎症反应的抗炎作用，而用渥曼青霉素（PI3K抑制剂）进行的AR809治疗则明显逆转了这种炎症反应。AR809可能通过调节TLR / PI3K / Akt / mTOR信号通路相关的自噬和TLR / PI3K / Akt /IκB/NF-κB通路活性来预防金黄色葡萄球菌引起的咽部炎症反应，
更新日期：2020-02-13
中文翻译：
人源唾液乳杆菌AR809可通过Akt介导的NF-κB和自噬信号通路防止金黄色葡萄球菌诱导的咽炎中的免疫抑制。
唾液乳杆菌AR809是一种新发现的益生菌菌株，来自健康的人类咽部，具有潜在的粘附咽上皮和抑制金黄色葡萄球菌（S. aureus）诱导的炎症反应的能力。喷洒AR809的咽部喷雾剂在金黄色葡萄球菌诱导的咽炎小鼠模型中显示出保护作用。进一步研究了AR809对金黄色葡萄球菌刺激的咽炎的抑制作用及其潜在的分子机制。AR809显着增加了吞噬作用和杀菌活性，减少了炎症介质的产生（细胞内活性氧（ROS），前列腺素E2（PGE2），环氧合酶2（COX-2），一氧化氮（NO），诱导型NOS（iNOS））和炎性细胞因子（肿瘤坏死因子-α（TNF-α）和白介素-1β（IL-1β））的表达，并诱导巨噬细胞采用M2表型。AR809还减弱了金黄色葡萄球菌诱导的蛋白激酶B（Akt）和雷帕霉素（mTOR）的磷酸化，并提高了自噬蛋白（II轻链3（LC3-II）和Beclin-1）的水平。此外，AR809通过抑制NF-κBp65的核转运来抑制核转录因子kappa-B（NF-κB）活化。同样，740Y-P（PI3K激活剂）降低了AR809对金黄色葡萄球菌诱导的炎症反应的抗炎作用，而用渥曼青霉素（PI3K抑制剂）进行的AR809治疗则明显逆转了这种炎症反应。AR809可能通过调节TLR / PI3K / Akt / mTOR信号通路相关的自噬和TLR / PI3K / Akt /IκB/NF-κB通路活性来预防金黄色葡萄球菌引起的咽部炎症反应，
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