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首页> 外文期刊>Infection and immunity >Subtractive Hybridization Identifies a Novel Predicted Protein Mediating Epithelial Cell Invasion by Virulent Serotype III Group B Streptococcus agalactiae
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Subtractive Hybridization Identifies a Novel Predicted Protein Mediating Epithelial Cell Invasion by Virulent Serotype III Group B Streptococcus agalactiae

机译：消减杂交确定了一种新的预测的蛋白介导的强毒血清型III B组链球菌无性上皮细胞的侵袭。

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Group B Streptococcus agalactiae bacteria (group B streptococci [GBS]) are the most common cause of serious bacterial infection in newborn infants. The majority of serotype III-related cases of neonatal disease are caused by a genetically related subgroup of bacteria, restriction fragment digest pattern (RDP) type III-3, suggesting that these strains possess unique genes contributing to virulence. We used genomic subtractive hybridization to identify regions of genomic DNA unique to virulent RDP type III-3 GBS strains. Within one of these III-3-specific regions is a 1,506-bp open reading frame, spb1 (surface protein of group B streptococcus 1). A mutant type III GBS strain lacking Spb1 was constructed in virulent RDP type III-3 strain 874391, and the interactions of the wild-type and spb1 isogenic mutant with a variety of epithelial cells important to GBS colonization and infection were compared. While adherence of the spb1 isogenic mutant to A549 respiratory, C2Bbe1 colonic, and HeLa cervical epithelial cells was slightly lower than that of the 874391 strain, invasion of the Spb1? mutant was significantly reduced with these cell lines compared to what was seen with 874391. The defect in epithelial invasion was corrected by supplying spb1 in trans. These observations suggest that Spb1 contributes to the pathogenesis of neonatal GBS infection by mediating internalization of virulent serotype III GBS and confirm that understanding of the population structure of bacteria may lead to insights into the pathogenesis of human infections.
机译：B组无乳链球菌细菌（B组链球菌[GBS]）是新生儿严重细菌感染的最常见原因。大多数与血清型III相关的新生儿疾病病例是由细菌的遗传相关亚组（限制性片段消化模式（RDP）III-3型）引起的，这表明这些菌株具有有助于致病性的独特基因。我们使用基因组消减杂交来鉴定具有毒力的RDP III-3型GBS菌株独特的基因组DNA区域。在这些III-3-特异区域之一中，有一个1,506 bp的开放阅读框 spb1 （B组链球菌1的表面蛋白）。在强毒的RDP III-3型菌株874391中构建了一个缺少Spb1的III型突变型GBS菌株，并且野生型和 spb1 等基因突变体与多种对GBS定殖和形成重要的上皮细胞的相互作用比较感染情况。虽然 spb1 等位基因突变体对A549呼吸道，C2Bbe1结肠和HeLa宫颈上皮细胞的粘附性略低于874391菌株，但对Spb1 ？突变体的侵袭却很严重。与874391相比，这些细胞系显着减少。通过在 trans 中提供 spb1 可以纠正上皮浸润的缺陷。这些观察结果表明，Spb1通过介导有毒的血清型III GBS的内在化而有助于新生儿GBS感染的发病机理，并证实对细菌种群结构的了解可能导致对人类感染的发病机理的了解。

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