肺炎克雷伯菌
微生物学
克雷伯菌
肠道菌群
肺
多糖
脂多糖
肠杆菌科
生物
细菌
医学
肺炎克雷伯菌
化学
肝损伤
急性胃肠炎
胞外多糖
免疫学
炎症
肺部感染
免疫系统
作者
Yifei Xiang,Shuxin Zhu,Renhe Wang,Jingsheng Huang,Han Li,Dejia Dai,Yunmei Yang,Hao Hu,Yingyi Wei,Tingjun Hu,Jiakang He,正敏 梁
出处
期刊:Food & Function
[Royal Society of Chemistry]
日期:2026-01-01
卷期号:17 (11): 5032-5046
摘要
< 0.05). Mechanistically, PCP restored intestinal barrier function by upregulating tight junction proteins (occludin and claudin-1) and mucosal defense factors (SIgA and MUC-2), and reversed gut dysbiosis by restoring microbial diversity and enriching beneficial taxa. These protective effects were largely attenuated in pseudo-germ-free mice, suggesting that the protection offered by PCP against MDR-KP-induced ALI is dependent on the gut microbiota. In conclusion, oral PCP alleviates MDR-KP-induced ALI through a gut microbiota-mediated pathway by remodeling the gut microbiota, reinforcing intestinal barrier integrity, and regulating the gut-lung axis, providing a novel gut-targeted therapeutic strategy against drug-resistant KP infections.
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