Role of the Emp Pilus Subunits of Enterococcus faecium in Biofilm Formation, Adherence to Host Extracellular Matrix Components, and Experimental Infection.
Role of the Emp Pilus Subunits of Enterococcus faecium in Biofilm Formation, Adherence to Host Extracellular Matrix Components, and Experimental Infection.
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屎肠球菌 Emp 菌毛亚基在生物膜形成、宿主细胞外基质成分粘附和实验感染中的作用。
DOI：
10.1128/iai.01396-15
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发表时间：
2016
影响因子：
3.1
通讯作者：
Murray,BarbaraE
中科院分区：
文献类型：
--
作者：
Montealegre,MariaCamila;Singh,KavindraV;Somarajan,SudhaR;Yadav,Puja;Chang,Chungyu;Spencer,Robert;Sillanpää,Jouko;Ton-That,Hung;Murray,BarbaraE
屎肠球菌是医院相关感染的重要原因，包括尿路感染（UTI）、菌血症和感染性心内膜炎。皮利已被证明在革兰氏阳性菌（包括E.屎室我们以前证明了一个无毛的ΔempABC：：catderivatives的E。屎肠TX 82在生物膜形成和UTI模型中被减弱。在这里，我们研究了单个菌毛亚基EmpA、EmpB和EmpC对菌毛结构、生物膜形成、粘附细胞外基质（ECM）蛋白和感染的贡献。我们鉴定了EmpA作为皮利的尖端，并发现缺失EmpA使生物膜形成减少到与缺失EmpAB Coperon相同的水平，这是一种通过原位重建EmpA基因而恢复的表型。empB的缺失也导致生物膜的减少，而EmpC被发现是不稳定的。在删除empA和empB后，观察到纤维蛋白原和I型胶原的粘附显著减少，而删除empChad后，没有粘附缺陷。此外，我们发现，在混合接种物UTI模型中，与同基因亲本菌株TX 82相比，每个缺失突变株均显著减毒（P< 0.001至0.048），在UTI模型中，重组empA恢复了毒力，在感染性心内膜炎模型中，empA缺失也导致减毒（P= 0.0088）。我们的研究结果表明，EmpA和EmpB，而不是EmpC，有助于生物膜和粘附ECM蛋白;然而，所有的Emp菌毛蛋白是重要的E。引起泌尿道感染。
Enterococcus faecium is an important cause of hospital-associated infections, including urinary tract infections (UTIs), bacteremia, and infective endocarditis. Pili have been shown to play a role in the pathogenesis of Gram-positive bacteria, including E. faecium. We previously demonstrated that a nonpiliated ΔempABC::catderivative of E. faecium TX82 was attenuated in biofilm formation and in a UTI model. Here, we studied the contributions of the individual pilus subunits EmpA, EmpB, and EmpC to pilus architecture, biofilm formation, adherence to extracellular matrix (ECM) proteins, and infection. We identified EmpA as the tip of the pili and found that deletion ofempAreduced biofilm formation to the same level as deletion of theempABCoperon, a phenotype that was restored by reconstitutingin situtheempAgene. Deletion ofempBalso caused a reduction in biofilm, while EmpC was found to be dispensable. Significant reductions in adherence to fibrinogen and collagen type I were observed with deletion ofempAandempB, while deletion ofempChad no adherence defect. Furthermore, we showed that each deletion mutant was significantly attenuated in comparison to the isogenic parental strain, TX82, in a mixed-inoculum UTI model (P< 0.001 to 0.048), that reconstitution ofempArestored virulence in the UTI model, and that deletion ofempAalso resulted in attenuation in an infective endocarditis model (P= 0.0088). Our results indicate that EmpA and EmpB, but not EmpC, contribute to biofilm and adherence to ECM proteins; however, all the Emp pilins are important for E. faecium to cause infection in the urinary tract.