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Antimicrobial peptide resistance mediates resilience of prominent gut commensals during inflammation

机译:抗菌肽抗性在炎症过程中介导重要肠道功能恢复

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摘要

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.
机译:抵抗宿主炎症和其他干扰的能力是肠道微生物群落的基本特性,但其潜在机制尚未得到很好的理解。我们发现来自所有显性门的人类肠道微生物对高水平的炎症相关抗微生物肽(AMP)具有抵抗力,并确定了拟杆菌门中脂多糖(LPS)修饰的机制将AMP抗性提高了四个数量级。在病原体感染引发的炎症过程中,未能从其LPS中去除单个磷酸基的拟杆菌拟南芥突变体已从微生物群中移出。这些发现建立了一种机制,可确定扰动过程中健康微生物群重要成员的稳定性。

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