Cullen T W, Schofield W B, Barry N A, Putnam E E, Rundell E A, Trent M S, Degnan P H, Booth C J, Yu H, Goodman A L
Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520, USA. Microbial Sciences Institute, Yale University School of Medicine, New Haven, CT 06520, USA.
Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520, USA.
Science. 2015 Jan 9;347(6218):170-5. doi: 10.1126/science.1260580.
Resilience to host inflammation and other perturbations is a fundamental property of gut microbial communities, yet the underlying mechanisms are not well understood. We have found that human gut microbes from all dominant phyla are resistant to high levels of inflammation-associated antimicrobial peptides (AMPs) and have identified a mechanism for lipopolysaccharide (LPS) modification in the phylum Bacteroidetes that increases AMP resistance by four orders of magnitude. Bacteroides thetaiotaomicron mutants that fail to remove a single phosphate group from their LPS were displaced from the microbiota during inflammation triggered by pathogen infection. These findings establish a mechanism that determines the stability of prominent members of a healthy microbiota during perturbation.
对宿主炎症和其他干扰的恢复力是肠道微生物群落的一项基本特性,但其潜在机制尚未得到充分理解。我们发现,所有主要门类的人类肠道微生物都对高水平的炎症相关抗菌肽(AMPs)具有抗性,并在拟杆菌门中确定了一种脂多糖(LPS)修饰机制,该机制可使AMPs抗性提高四个数量级。在病原体感染引发的炎症期间,无法从其LPS上去除单个磷酸基团的多形拟杆菌突变体从微生物群中被取代。这些发现建立了一种机制,该机制决定了健康微生物群中重要成员在受到干扰时的稳定性。