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荚膜多糖是大肠杆菌K-1阳性血培养分离株血清抗性的主要决定因素。

The capsular polysaccharide is a major determinant of serum resistance in K-1-positive blood culture isolates of Escherichia coli.

作者信息

Leying H, Suerbaum S, Kroll H P, Stahl D, Opferkuch W

机构信息

Abteilung für Medizinische Mikrobiologie und Immunologie, Ruhr-Universität Bochum, Federal Republic of Germany.

出版信息

Infect Immun. 1990 Jan;58(1):222-7. doi: 10.1128/iai.58.1.222-227.1990.

Abstract

Serum resistance is a major virulence factor of gram-negative bacteria, and K-1 polysaccharide has been shown to contribute to serum resistance in selected strains. To obtain further information about the role of K-1 in serum resistance and to find out whether loss of the ability to produce K-1 can induce loss of serum resistance, we studied the serum resistance of mutants derived from completely serum-resistant, K-1-positive blood culture isolates of Escherichia coli by selection for resistance to infection with K-1 specific bacteriophages. The amounts of K-1 polysaccharide produced by wild-type strains and mutants were measured, and outer membrane protein and lipopolysaccharide (LPS) patterns were analyzed. In each group of mutants, several highly serum-sensitive strains were found. All mutant strains expressed less K-1 than did the corresponding wild-type strains. Mutants that became highly serum sensitive always had less K-1 than did mutants with less-pronounced changes of serum resistance. A few mutants derived from different wild-type strains showed increased expression of outer membrane proteins with molecular weights of about 46,000 and 67,000. All of the wild-type strains examined had smooth-type LPS, and only two mutants had altered LPS structures; alterations of mutants in outer membrane proteins and LPS could not be correlated with alterations of serum resistance. The results indicate that for K-1-positive blood culture strains of E. coli, K-1 expression is a prerequisite for serum resistance, and loss of ability to synthesize K-1 leads to loss of serum resistance.

摘要

血清抗性是革兰氏阴性菌的一个主要毒力因子,并且已表明K-1多糖在特定菌株中有助于血清抗性。为了获得关于K-1在血清抗性中作用的更多信息,并弄清楚产生K-1能力的丧失是否会导致血清抗性的丧失,我们通过选择对K-1特异性噬菌体感染具有抗性,研究了源自完全血清抗性、K-1阳性大肠杆菌血培养分离株的突变体的血清抗性。测定了野生型菌株和突变体产生的K-1多糖量,并分析了外膜蛋白和脂多糖(LPS)模式。在每组突变体中,发现了几种高度血清敏感的菌株。所有突变菌株表达的K-1都比相应的野生型菌株少。变得高度血清敏感的突变体总是比血清抗性变化不明显的突变体具有更少的K-1。少数源自不同野生型菌株的突变体显示分子量约为46,000和67,000的外膜蛋白表达增加。所有检测的野生型菌株都具有光滑型LPS,只有两个突变体的LPS结构发生了改变;突变体在外膜蛋白和LPS方面的改变与血清抗性的改变无关。结果表明,对于K-1阳性的大肠杆菌血培养菌株,K-1表达是血清抗性的先决条件,合成K-1能力的丧失导致血清抗性的丧失。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5b0/258433/e954aac21857/iai00049-0241-a.jpg

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