SURVIVAL AND IMPLANTATION OF ESCHERICHIA-COLI IN THE INTESTINAL-TRACT
SURVIVAL AND IMPLANTATION OF ESCHERICHIA-COLI IN THE INTESTINAL-TRACT
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DOI：
10.1128/iai.39.2.686-703.1983
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发表时间：
1983-01-01
影响因子：
3.1
通讯作者：
CAREY, KE
中科院分区：
文献类型：
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作者：
FRETER, R;BRICKNER, H;CAREY, KE
将0.5 ml接种物直接注入小鼠胃内，可迅速清除进入小肠。碳酸氢盐缓冲液，而不是脱脂牛奶，保护这样的接种物免受胃酸的侵害，直到至少90%的胃酸进入小肠。将两种肠道示踪剂（Cr51Cl3和一种嗜热芽孢杆菌孢子）直接注入小鼠胃中，检测不同大肠杆菌菌株在小鼠肠道中的传代和存活。将粪便在冷藏笼中收集过夜，定量回收排泄细菌。野生型大肠杆菌和大肠杆菌K-12在18 h内迅速从粪便中排出（98-100%），没有整体增殖或死亡。大肠杆菌。1776和DP50supF，即经过重组DNA实验认证的菌株，在体内迅速死亡，粪便中的排泄量减少到约0.75%。分别占接种量的1.1%和4.7%。胃的酸度对大肠杆菌K-12菌株几乎没有杀菌作用，但在这些条件下显著降低了对酸敏感的细菌（霍乱弧菌）的存活率。将大肠杆菌菌株长期植入小鼠盲肠菌群连续培养物或常规小鼠体内是困难的。当大肠杆菌菌株首次接种于无菌CF培养物或无菌小鼠（随后与常规小鼠盲肠菌群相关）时，大肠杆菌菌株在很大比例的动物中持续存在，其水平与常规小鼠中的大肠杆菌种群相似。首先引入的大肠杆菌接种物的成功，代谢适应只起到了部分作用。描述了一个数学模型，该模型解释了基于粘附位点竞争的这种现象，在这种竞争中，首先占据这些位点的细菌具有优势。该数学模型预测，如果代谢效率较低的菌株具有特定的粘附位点，那么在肠道中竞争相同限制营养物质的两种细菌菌株可以共存。大肠杆菌在单菌共生小鼠体内的生长比速率常数为2.0 h-1；常规动物排泄率为-0.23 h-1。因此，限制生长一定是控制大肠细菌数量的主要机制。提出了大肠生态学的一般假设的开端，其中先前描述的竞争性代谢相互作用的影响被细菌与肠壁结合的影响所修改。
A 0.5 ml inoculum introduced directly into the stomach of mice was cleared rapidly into the small intestine. Bicarbonate buffer, but not skim milk, protected such an inoculum from stomach acid until at least 90% of it had entered the small intestine. Passage and survival of various E. coli strains through the mouse gut were tested by introducing a buffered bacterial inoculum directly into the stomach with the following 2 intestinal tracers: Cr51Cl3 and spores of a thermophilic Bacillus sp. Quantitative recovery of excreted bacteria was accomplished by collecting the feces overnight in a refrigerated cage pan. Wild-type E. coli strains and E. coli K-12 were excreted rapidly (98-100% within 18 h) in the feces without overall multiplication or death. E. coli .chi. 1776 and DP50supF, i.e., strains certified for recombinant DNA experiments, underwent rapid death in vivo such that their excretion in the feces was reduced to .apprx. 1.1 and 4.7% of the inoculum, respectively. The acidity of the stomach had little bactericidal effect on the E. coli K-12 strain tested, but significantly reduced the survival of more acid-sensitive bacteria (Vibrio cholerae) under these conditions. Long-term implantation of E. coli strains into continuous-flow [CF] cultures of mouse cecal flora or into conventional mice was difficult. When the E. coli strain was first inoculated into sterile CF cultures or into germfree mice, which were subsequently associated with conventional mouse cecal flora, the E. coli strains persisted in a large proportion of the animals at levels resembling E. coli populations in conventional mice. Metabolic adaptation contributed only partially to the success of an E. coli inoculum that was first introduced. A mathematical model is described which explains this phenomenon on the basis of competition for adhesion sites, in which an advantage accrues to the bacterium which occupies those sites first. The mathematical model predicts that 2 bacterial strains that compete in the gut for the same limiting nutrient can coexist if the metabolically less efficient strains have specific adhesion sites available. The specific rate constant of E. coli growth in monoassociated gnotobiotic mice was 2.0 h-1; the excretion rate in conventional animals was -0.23 h-1. Consequently, limitation of growth must be the primary mechanism controlling bacterial populations in the large intestine. The beginnings of a general hypothesis of the ecology of the large intestine are proposed, in which the effects of the competitive metabolic interactions described earlier are modified by the effects of bacterial association with the intestinal wall.