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首页> 外文期刊>Infection and immunity >An Abundance of Escherichia coli Is Harbored by the Mucosa- Associated Bacterial Flora of Interleukin-2-Deficient Mice
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An Abundance of Escherichia coli Is Harbored by the Mucosa- Associated Bacterial Flora of Interleukin-2-Deficient Mice

机译：白细胞介素2缺陷型小鼠的粘膜相关细菌菌群带有大量的大肠杆菌。

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Mice deficient in interleukin-2 are well suited for use as an animal model for inflammatory bowel disease. Raised under specific-pathogen-free conditions, interleukin-2-deficient mice develop an inflammatory bowel disease resembling ulcerative colitis in humans. The finding that colitis was attenuated when the mice were kept under germfree conditions implies that the resident intestinal flora is involved in the pathogenesis of colitis. The present study addresses the composition of the mucosa-associated bacterial flora in colon samples from interleukin-2-deficient mice that developed colitis. This was investigated by comparative 16S ribosomal DNA (rDNA) sequence analysis and fluorescence in situ hybridization using rRNA-targeted fluorescent probes to quantify the bacterial populations of the mucosa-associated flora. The investigations revealed distinct differences in the bacterial composition of the mucosa-associated flora between interleukin-2-deficient mice and healthy controls. Fluorescence in situ hybridization identified up to 10% of the mucosa-associated flora in interleukin-2-deficient mice as Escherichia coli, whereas no E. coli was detected in the mucosa from healthy wild-type mice. This finding was consistent with the results from comparative 16S rDNA analysis. About one-third of the clones analyzed from 16S rDNA libraries of interleukin-2-deficient mice represented Enterobacteriaceae, whereas none of the clones analyzed from the healthy controls harbored 16S rDNA from Enterobacteriaceae. The abundance of E. coli in the colonic mucosa of interleukin-2-deficient mice strongly suggests a participation in the pathogenesis of colitis in the interleukin-2-deficient mouse model for inflammatory bowel disease.
机译：缺乏白细胞介素2的小鼠非常适合用作炎症性肠病的动物模型。在无特定病原体的条件下饲养的白介素2缺乏症小鼠会出现类似于人类溃疡性结肠炎的炎症性肠病。当将小鼠置于无菌条件下时，结肠炎被减弱的发现表明，常驻肠道菌群参与了结肠炎的发病机理。本研究解决了结肠炎中白介素2缺陷型小鼠结肠样本中与粘膜相关的细菌菌群的组成。这是通过比较16S核糖体DNA（rDNA）序列分析和使用rRNA靶向的荧光探针进行荧光原位杂交研究来量化与粘膜相关菌群的细菌种群的。研究发现白介素2缺陷型小鼠与健康对照组之间粘膜相关菌群的细菌组成存在明显差异。荧光原位杂交鉴定出白介素2缺陷型小鼠中粘膜相关菌群中多达10％为大肠杆菌，而没有 E。在健康的野生型小鼠的粘膜中检测到大肠杆菌。这一发现与比较16S rDNA分析的结果一致。从白介素2缺陷型小鼠的16S rDNA文库分析的克隆中约有三分之一代表肠杆菌科，而从健康对照中分析出的克隆均没有来自肠杆菌科的16S rDNA。 >。 E的丰度。白介素2缺陷型小鼠结肠黏膜中的大肠杆菌强烈提示参与白细胞介素2缺陷型炎性肠病小鼠结肠炎的发病机理。

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