Background and Purpose. Allergic asthma, a respiratory disease with high morbidity and mortality, is reported to be related to the airway allergic inflammation and autophagy-induced oxidative stress. Although the therapeutic effects of fermentate prebiotic (YFP) on allergic asthma have been widely claimed, the underlying mechanism is still unclear. This study is aimed at investigating the possible mechanism for the antiasthma property of YFP in a mouse model. Methods. Ovalbumin was used to induce allergic asthma following administration of YFP for one week in mice, to collect the lung tissues, bronchoalveolar lavage fluid (BLFA), and feces. The pathological state, tight-junction proteins, inflammatory and oxidative stress-associated biomarkers, and TLRs/NF-κB signaling pathway of the lung tissues were evaluated by HE staining, immunofluorescence, ELISA, and WB, separately. RT-PCR was used to test oxidative stress-associated genes. Leukocyte counts of BLFA and intestinal microbiota were also analyzed using a hemocytometer and 16S rDNA-sequencing, separately. Result. YFP ameliorated the lung injury of the mouse asthma model by inhibiting peribronchial and perivascular infiltrations of eosinophils and increasing tight-junction protein expression. YFP inhibited the decrease in the number of BALF leukocytes and expression of inflammatory-related genes and reversed OVA-induced TLRs/NF-κB signaling pathway activation. YFP ameliorated the level of oxidative stress in the lung of the mouse asthma model by inhibiting MDA and promoting the protein level of GSH-PX, SOD, CAT, and oxidative-related genes. ATG5, Beclin1, and LC3BII/I were significantly upregulated in asthma mice, which were greatly suppressed by the introduction of YFP, indicating that YFP ameliorated the autophagy in the lung of the mouse asthma model. Lastly, the distribution of bacterial species was slightly changed by YFP in asthma mice, with a significant difference in the relative abundance of 6 major bacterial species between the asthma and YFP groups. Conclusion. Our research showed that YFP might exert antiasthmatic effects by inhibiting airway allergic inflammation and oxidative stress level through suppressing autophagy.

中文翻译：

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酵母发酵益生元改善过敏性哮喘，通过抑制自噬与抑制炎症和降低氧化应激水平相关

背景和目的。过敏性哮喘是一种发病率和死亡率高的呼吸道疾病，据报道与气道过敏性炎症和自噬诱导的氧化应激有关。尽管发酵益生元 (YFP) 对过敏性哮喘的治疗作用已广为人知，但其潜在机制仍不清楚。本研究旨在研究 YFP 在小鼠模型中抗哮喘特性的可能机制。方法。YFP 给药 1 周后，用卵清蛋白诱导小鼠过敏性哮喘，收集肺组织、支气管肺泡灌洗液 (BLFA) 和粪便。病理状态、紧密连接蛋白、炎症和氧化应激相关生物标志物以及 TLR/NF- κ分别通过HE染色、免疫荧光、ELISA和WB评估肺组织的B信号通路。RT-PCR 用于测试氧化应激相关基因。还分别使用血细胞计数器和 16S rDNA 测序分析了 BLFA 和肠道微生物群的白细胞计数。结果。YFP通过抑制嗜酸性粒细胞的支气管周围和血管周围浸润和增加紧密连接蛋白的表达来改善小鼠哮喘模型的肺损伤。YFP 抑制 BALF 白细胞数量和炎症相关基因表达的减少，并逆转 OVA 诱导的 TLRs/NF- κB信号通路激活。YFP 通过抑制 MDA 并提高 GSH-PX、SOD、CAT 和氧化相关基因的蛋白水平来改善小鼠哮喘模型肺中的氧化应激水平。ATG5、Beclin1 和 LC3BII/I 在哮喘小鼠中显着上调，而 YFP 的引入大大抑制了这些表达，表明 YFP 改善了小鼠哮喘模型肺中的自噬。最后，YFP 在哮喘小鼠中的细菌种类分布略有改变，哮喘组和 YFP 组之间 6 种主要细菌种类的相对丰度存在显着差异。结论。我们的研究表明，YFP 可能通过抑制自噬来抑制气道过敏性炎症和氧化应激水平，从而发挥平喘作用。