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荚膜缺失或死亡:荚膜基因中突变的位置决定了猪链球菌的命运。

Capsule loss or death: the position of mutations among capsule genes sways the destiny of Streptococcus suis.

作者信息

Lakkitjaroen Nattakan, Takamatsu Daisuke, Okura Masatoshi, Sato Masumi, Osaki Makoto, Sekizaki Tsutomu

机构信息

Research Center for Food Safety, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.

出版信息

FEMS Microbiol Lett. 2014 May;354(1):46-54. doi: 10.1111/1574-6968.12428. Epub 2014 Apr 3.

DOI:10.1111/1574-6968.12428
PMID:24654559
Abstract

Streptococcus suis, an emerging zoonotic pathogen, is responsible for various diseases in swine and humans. Most S. suis strains from clinical cases possess a group of capsular polysaccharide synthesis (cps) genes and phenotypically express capsular polysaccharides (CPs). Although CPs are considered to be an important virulence factor, our previous study showed that many S. suis isolates from porcine endocarditis lost their CPs, and some of these unencapsulated isolates had large insertions or deletions in the cps gene clusters. We further investigated 25 endocarditis isolates with no obvious genetic alterations to elucidate the unencapsulation mechanisms and found that a single-nucleotide substitution and frameshift mutation in two glycosyltransferase genes (cps2E and cps2F) were the main causes of the capsule loss. Moreover, mutations in the genes involved in side-chain formation (cps2J and cps2N), polymerase (cps2I), and flippase (cps2O) appeared to be lethal; however, these lethal effects were relieved by mutations in the cps2EF region. As unencapsulation and even the death of individual cells have recently been suggested to be beneficial to the pathogenesis of infections, the results of the present study provide a further insight into understanding the biological significance of cps mutations during the course of S. suis infections.

摘要

猪链球菌是一种新出现的人畜共患病原体,可导致猪和人类的多种疾病。大多数临床病例中的猪链球菌菌株拥有一组荚膜多糖合成(cps)基因,并在表型上表达荚膜多糖(CPs)。尽管CPs被认为是一种重要的毒力因子,但我们之前的研究表明,许多来自猪心内膜炎的猪链球菌分离株失去了它们的CPs,并且这些无荚膜分离株中的一些在cps基因簇中存在大的插入或缺失。我们进一步研究了25株无明显基因改变的心内膜炎分离株,以阐明无荚膜形成机制,发现两个糖基转移酶基因(cps2E和cps2F)中的单核苷酸取代和移码突变是荚膜丧失的主要原因。此外,参与侧链形成(cps2J和cps2N)、聚合酶(cps2I)和翻转酶(cps2O)的基因中的突变似乎是致命的;然而,这些致命效应通过cps2EF区域的突变得以缓解。由于最近有人提出无荚膜甚至单个细胞的死亡对感染的发病机制有益,本研究结果为深入了解猪链球菌感染过程中cps突变的生物学意义提供了进一步的见解。

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