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一种与坏死性小肠结肠炎相关的细菌致病性决定因素。

A bacterial pathogenicity determinant associated with necrotizing enterocolitis.

作者信息

Carbonaro C A, Clark D A, Elseviers D

机构信息

Department of Microbiology and Immunology, New York Medical College, Valhalla 10595.

出版信息

Microb Pathog. 1988 Dec;5(6):427-36. doi: 10.1016/0882-4010(88)90004-6.

Abstract

Predominant enterobacteria from infants with necrotizing enterocolitis (NEC) were examined for an unusual ability to ferment lactose. One such isolate, a Klebsiella pneumoniae strain, was partially induced for lactose operon expression in tryptone containing media, and was also pathogenic in a rabbit ileal loop model for NEC. A spontaneous segregant of this strain was no longer partially induced for lactose operon expression, and was no longer pathogenic in the rabbit model. The gene responsible for this phenotype was cloned. The resulting plasmid was shown to cause both partially induced lactose operon expression and pathogenicity when introduced into a laboratory K. pneumoniae strain. A K. pneumoniae mutant deficient in lactose repressor synthesis was also pathogenic in the rabbit model. These results and previous studies on the intraluminal biochemistry of infants with NEC support the hypothesis that an increased ability for lactose fermentation may be a bacterial pathogenic trait with respect to NEC.

摘要

对坏死性小肠结肠炎(NEC)婴儿的主要肠道杆菌进行了乳糖发酵异常能力的检测。其中一株分离菌,即肺炎克雷伯菌菌株,在含胰蛋白胨的培养基中乳糖操纵子表达被部分诱导,并且在NEC的兔回肠袢模型中具有致病性。该菌株的一个自发分离株不再被部分诱导乳糖操纵子表达,并且在兔模型中不再具有致病性。负责这种表型的基因被克隆。当将所得质粒引入实验室肺炎克雷伯菌菌株时,显示其可导致乳糖操纵子的部分诱导表达和致病性。乳糖阻遏物合成缺陷的肺炎克雷伯菌突变体在兔模型中也具有致病性。这些结果以及先前关于NEC婴儿肠腔内生物化学的研究支持了这样一种假说,即乳糖发酵能力的增强可能是与NEC相关的细菌致病特性。

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