Probiotic E-coli treatment mediates antimicrobial human β-defensin synthesis and fecal excretion in humans

被引:128
作者
Moendel, M. [1 ,2 ]
Schroeder, B. O. [1 ,2 ]
Zimmermann, K. [3 ]
Huber, H. [4 ]
Nuding, S. [1 ,2 ]
Beisner, J. [1 ,2 ]
Fellermann, K. [5 ]
Stange, E. F. [5 ]
Wehkamp, J. [1 ,2 ,5 ]
机构
[1] Dr Margarete Fischer Bosch Inst Clin Pharmacol, D-7000 Stuttgart, Germany
[2] Univ Tubingen, Stuttgart, Germany
[3] Symbio Herborn Grp GmbH, Herborn, Germany
[4] Inst Microecol, Herborn, Germany
[5] Robert Bosch Krankenhaus, Dept Internal Med 1, Stuttgart, Germany
关键词
NISSLE; 1917; MAINTAINING REMISSION; ULCERATIVE-COLITIS; PEPTIDES; MESALAZINE; INDUCTION; DIARRHEA; INFANTS;
D O I
10.1038/mi.2008.77
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Inducible epithelial human beta-defensins (hBD) play an important role in intestinal barrier function. In vitro studies showed that clinically effective probiotics induce antimicrobial hBD-2. Here, we aimed to assess the in vivo effect in healthy volunteers and also addressed how defensins affect probiotic survival. Symbioflor 2 containing one strain of several viable genotypes of Escherichia coli was administered to 23 healthy individuals. After 3 weeks, fecal hBD-2 peptide was increased in 78% ( mean 3.7-fold; P<0.0001). Interestingly, the fecal hBD-2 peptide was still elevated 9 weeks after treatment (P=0.008). In vitro studies revealed that this effect was mediated by only one out of three tested E. coli genotypes and comparable to probiotic E. coli Nissle 1917 (10- to 15-fold). Functional assays showed that all tested bacteria were similarly killed by defensins allowing to speculate about a suicidal character of this effect. Defensin induction seems to be a common and important mechanism of probiotic treatment.
引用
收藏
页码:166 / 172
页数:7
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