脆弱类杆菌
使负有责任或义务
专性厌氧菌
生物
微生物学
毒力
病菌
拟杆菌
氧化磷酸化
毒力因子
厌氧糖酵解
无氧运动
厌氧菌
细菌
新陈代谢
糖酵解
基因
生态学
生物化学
遗传学
生理学
抗生素
作者
Luisella Spiga,Ryan T. Fansler,Alexandra Grote,Madison Langford-Butler,Asia K. Miller,M J Neal,Owen F. Hale,Yifan Wu,Deepanshu Singla,M. Wade Calcutt,Abigail E. Rose,Madeline M. Bresson,Alexandra C. Schrimpe‐Rutledge,Brittany Berdy,Simona G. Codreanu,M. Kay Washington,Benjamin P. Bratton,Stacy D. Sherrod,John A. McLean,Karsten Zengler
标识
DOI:10.1101/2025.05.31.657111
摘要
toxin activates colonic epithelial signaling and hijacks the host bile acid recycling pathway, inducing a metabolic shift in the epithelium from oxidative phosphorylation to glycolysis. This shift increases local concentrations of lactate and oxygen, nutrients that support an oxidative metabolism in ETBF. These findings reveal an unexpected strategy by which a pathogenic organism, previously considered to be an obligate anaerobic bacterium, generates and exploits an oxidative niche in the inflamed gut.
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