Nutritional basis for colonization resistance by human commensal Escherichia coli strains HS and Nissle 1917 against E. coli O157:H7 in the mouse intestine.
Nutritional basis for colonization resistance by human commensal Escherichia coli strains HS and Nissle 1917 against E. coli O157:H7 in the mouse intestine.
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DOI：
10.1371/journal.pone.0053957
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Conway T
中科院分区：
文献类型：
--
作者：
Maltby R;Leatham-Jensen MP;Gibson T;Cohen PS;Conway T
大肠杆菌是由许多生物型组成的单一物种，其中一些是哺乳动物的肠道定植者，另一些则引起疾病。人类平均有五种寄生虫生物型，人们普遍认为寄生虫是病原体感染的屏障。先前的研究表明，三种预定殖的Escherosal E.大肠杆菌菌株阻止E.大肠杆菌O 157：H7的小鼠模型（Leatham，et al.，2010，Infect Immun 77：2876-7886）。该菌的生物型包括E.大肠杆菌HS，已知其在高剂量下成功地定殖于人类而没有副作用，以及E.大肠杆菌Nissle 1917，一种在欧洲用于预防旅行者腹泻的人类肠道菌株。我们推测，Escherichia coli生物型可能通过消耗E.大肠杆菌O 157：H7定殖，从而阻止感染的第一步。在这里，我们报告说，定殖链霉素治疗的小鼠E。大肠杆菌HS消耗12种糖中的6种，而E. coli Nissle 1917使用互补但不同的七种糖来定殖，从而为E. coli HS和Nissle 1917在小鼠肠道中占据不同的小生境。这两种糖共同使用五种糖，这五种糖以前被确定为对E. coliEDL 933，O 157：H7菌株。正如预测的那样，这两种药物阻止了E。coliEDL 933定殖。这些结果支持了一种致病性E.大肠杆菌必须与肠道微生物群竞争以获得定殖和建立感染所需的营养素;因此，挑战的结果取决于天然微生物群消耗病原体所需营养素的总能力。
Escherichia coli is a single species consisting of many biotypes, some of which are commensal colonizers of mammals and others that cause disease. Humans are colonized on average with five commensal biotypes, and it is widely thought that the commensals serve as a barrier to infection by pathogens. Previous studies showed that a combination of three pre-colonized commensal E. coli strains prevents colonization of E. coli O157:H7 in a mouse model (Leatham, et al., 2010, Infect Immun 77: 2876–7886). The commensal biotypes included E. coli HS, which is known to successfully colonize humans at high doses with no adverse effects, and E. coli Nissle 1917, a human commensal strain that is used in Europe as a preventative of traveler's diarrhea. We hypothesized that commensal biotypes could exert colonization resistance by consuming nutrients needed by E. coli O157:H7 to colonize, thus preventing this first step in infection. Here we report that to colonize streptomycin-treated mice E. coli HS consumes six of the twelve sugars tested and E. coli Nissle 1917 uses a complementary yet divergent set of seven sugars to colonize, thus establishing a nutritional basis for the ability of E. coli HS and Nissle 1917 to occupy distinct niches in the mouse intestine. Together these two commensals use the five sugars previously determined to be most important for colonization of E. coli EDL933, an O157:H7 strain. As predicted, the two commensals prevented E. coli EDL933 colonization. The results support a model in which invading pathogenic E. coli must compete with the gut microbiota to obtain the nutrients needed to colonize and establish infection; accordingly, the outcome of the challenge is determined by the aggregate capacity of the native microbiota to consume the nutrients required by the pathogen.
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影响因子：
3.1
作者：
FRETER, R;BRICKNER, H;CAREY, KE
通讯作者：
CAREY, KE
影响因子：
3.1
作者：
Jones, Shari A.;Gibson, Terri;Conway, Tyrrell
通讯作者：
Conway, Tyrrell
影响因子：
3.1
作者：
Jones, Shari A.;Jorgensen, Mathias;Conway, Tyrrell
通讯作者：
Conway, Tyrrell
影响因子：
3.1
作者：
Bryan, A;Roesch, P;Welch, RA
通讯作者：
Welch, RA
DOI：
10.1111/j.1749-6632.1971.tb35004.x
发表时间：
1971-01-01
影响因子：
5.2
作者：
FORMAL, SB;DUPONT, HL;LABREC, EH
通讯作者：
LABREC, EH