Abstract
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.
Highlights
Allergic asthma is a common chronic inflammatory respiratory disease with high morbidity and mortality all over the world
Hematoxylin and Eosin (HE) staining was used to check the pathological state of the lung tissues, and the immunofluorescence assay was used to determine the expression level of tight junctionrelated proteins
ZO-1, Claudin1, Claudin4, and Occludin were significantly downregulated in the asthma group, compared to the control, the expression of which was significantly promoted by the treatment of Yeast Fermentate Prebiotics (YFP) (Figures 1(b)–1(d))
Summary
Allergic asthma is a common chronic inflammatory respiratory disease with high morbidity and mortality all over the world. A respiratory disease with high morbidity and mortality, is reported to be related to the airway allergic inflammation and autophagy-induced oxidative stress. 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. Our research showed that YFP might exert antiasthmatic effects by inhibiting airway allergic inflammation and oxidative stress level through suppressing autophagy
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