Vancomycin-resistant Enterococcus domination of intestinal microbiota is enabled by antibiotic treatment in mice and precedes bloodstream invasion in humans

被引:680
作者
Ubeda, Caries [2 ]
Taur, Ying
Jenq, Robert R. [3 ]
Equinda, Michele J. [2 ]
Son, Tammy [3 ]
Samstein, Miriam [2 ]
Viale, Agnes [4 ]
Socci, Nicholas D. [5 ]
van den Brink, Marcel R. M. [2 ,3 ]
Kamboj, Mini
Pamer, Eric G. [1 ,2 ]
机构
[1] Mem Sloan Kettering Canc Ctr, Dept Med, Infect Dis Serv, Lab Antimicrobial Immun, New York, NY 10065 USA
[2] Sloan Kettering Inst, Program Immunol, New York, NY USA
[3] Mem Sloan Kettering Canc Ctr, Dept Med, Bone Marrow Transplant Serv, New York, NY 10065 USA
[4] Sloan Kettering Inst, Genom Core Lab, New York, NY USA
[5] Sloan Kettering Inst, Computat Biol Ctr, New York, NY USA
关键词
GUT MICROBIOTA; PANETH CELLS; COLONIZATION; DIVERSITY; ECOLOGY; SUSCEPTIBILITY; EXPRESSION; MORTALITY; INNATE; INDUCE;
D O I
10.1172/JCI43918
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Bloodstream infection by highly antibiotic-resistant bacteria, such as vancomycin-resistant Enterococcus (VRE), is a growing clinical problem that increasingly defies medical intervention. Identifying patients at high risk for bacterial sepsis remains an important clinical challenge. Recent studies have shown that antibiotics can alter microbial diversity in the intestine. Here, we characterized these effects using 16s rDNA pyrosequencing and demonstrated that antibiotic treatment of mice enabled exogenously administered VRE to efficiently and nearly completely displace the normal microbiota of the small and large intestine. In the clinical setting, we found that intestinal domination by VRE preceded bloodstream infection in patients undergoing allogeneic hematopoietic stem cell transplantation. Our results demonstrate that antibiotics perturb the normal commensal microbiota and set the stage for intestinal domination by bacteria associated with hospital-acquired infections. Thus, high-throughput DNA sequencing of the intestinal microbiota could identify patients at high risk of developing bacterial sepsis.
引用
收藏
页码:4332 / 4341
页数:10
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