Bacillus velezensis alleviates PM(2.5)-induced intestinal injury and dysbiosis in broilers via the "lung-gut axis"

贝莱斯芽孢杆菌通过“肺-肠轴”缓解PM(2.5)引起的肉鸡肠道损伤和菌群失调

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Abstract

BACKGROUND: This study investigated how tracheal instillation of Bacillus velezensis mitigates PM(2.5)-induced lung injury and counteracts its adverse effects on distal intestinal health in broilers via the "lung-gut axis". RESULTS: Five groups were randomly selected from among seventy-five 14-day-old AA broilers: Control, Saline, PM2.5, B. velezensis, and B. velezensis + PM2.5. Results showed that compared with the Saline group, PM(2.5) exposure disrupted lung structure and significantly upregulated TLR4, MyD88, NF-κB, IL-18, and IFN-γ related inflammatory factors via the TLR4/MyD88/NF-κB signaling axis (P < 0.05). In addition, it significantly reduced jejunal villus height through the action of the "lung-gut axis" (P < 0.05), decreased the levels of IL-10, Claudin-1, and Occludin while increasing that of IL-22 (P < 0.05). Analysis of the cecal microbiota found that PM(2.5) reduced the Shannon index of bacterial communities and raised the relative abundance of Bacteroidota, Pseudomonadota, and Flavonifractor. Co-treatment with B. velezensis + PM(2.5) reversed the above changes, significantly improved lung and intestinal morphology, enhanced jejunal barrier function, reduced lung and jejunal inflammatory responses, and increased the relative abundance of Faecalibacterium. Based on KEGG functional prediction, the PM(2.5) group was enriched in microbial metabolic pathways, such as two-component systems and ABC transporters. CONCLUSIONS: Tracheal instillation of B. velezensis can improve the expression of genes associated with lung injury via the TLR4/MyD88/NF-κB signaling axis and effectively alleviate PM(2.5)-induced distal jejunal damage, barrier dysfunction, inflammatory response, and dysbiosis by mediating the "lung-gut axis". This could provide a theoretical support and scientific basis for seeking probiotics to improve PM(2.5) harm.

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