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首页> 外文期刊>Journal of Medical Microbiology: An Official Journal of the Pathological Society of Great Britain and Ireland >Host factors abolish the need for polysaccharides and extracellular matrix-binding protein in Staphylococcus epidermidis biofilm formation
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Host factors abolish the need for polysaccharides and extracellular matrix-binding protein in Staphylococcus epidermidis biofilm formation

机译：宿主因子取消了在<斜体>葡萄球菌表皮中对多糖和细胞外基质结合蛋白的需要生物膜形成

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Introduction Staphylococcus epidermidis is predominant in implant-associated infections due to its capability to form biofilms. It can deploy several strategies for biofilm development using either polysaccharide intercellular adhesin (PIA), extracellular DNA (eDNA) and/or proteins, such as the extracellular matrix-binding protein (Embp). Hypothesis/Gap Statement We hypothesize that the dichotomic regulation of S. epidermidis adhesins is linked to whether it is inside a host or not, and that in vitro biofilm investigations in laboratory media may not reflect actual biofilms in vivo . Aim We address the importance of PIA and Embp in biofilm grown in ‘humanized’ media to understand if these components play different roles in biofilm formation under conditions where bacteria can incorporate host proteins in the biofilm matrix. Methodology S. epidermidis 1585?WT (deficient in icaADBC ), and derivative strains that either lack embp , express embp from an inducible promotor, or express icaADBC from a plasmid, were cultivated in standard laboratory media, or in media with human plasma or serum. The amount, structure, elasticity and antimicrobial penetration of biofilms was quantified to describe structural differences caused by the different matrix components and growth conditions. Finally, we quantified the initiation of biofilms as suspended aggregates in response to host factors to determine how quickly the cells aggregate in response to the host environment and reach a size that protects them from phagocytosis. Results S. epidermidis 1585 required polysaccharides to form biofilm in laboratory media. However, these observations were not representative of the biofilm phenotype in the presence of human plasma. If human plasma were present, polysaccharides and Embp were redundant for biofilm formation. Biofilms formed in human plasma were loosely attached and existed mostly as suspended aggregates. Aggregation occurred after 2?h of exposing cells to plasma or serum. Despite stark differences in the amount and composition of biofilms formed by polysaccharide-producing and Embp-producing strains in different media, there were no differences in vancomycin penetration or susceptibility. Conclusion. We suggest that the assumed importance of polysaccharides for biofilm formation is an artefact from studying biofilms in laboratory media void of human matrix components. The cell–cell aggregation of S. epidermidis can be activated by host factors without relying on either of the major adhesins, PIA and Embp, indicating a need to revisit the basic question of how S. epidermidis deploys self-produced and host-derived matrix components to form antibiotic-tolerant biofilms in vivo .
机译：由于其形成生物膜的能力，引言葡萄球菌表皮是植入物相关感染的主要感染。它可以使用多糖细胞间粘合剂（PIA），细胞外DNA（EDNA）和/或蛋白质，例如细胞外基质结合蛋白（embp）来部署几种生物膜开发策略。假设/间隙陈述我们假设S.表皮粘连素的二分调节与其在宿主内是否有关，并且在实验室培养基中的体外生物膜调查可能不会在体内反映实际的生物膜。旨在解决PIA和Embp在“人源化”媒体中生物膜的重要性，了解这些组分在细菌在生物膜基质中掺入宿主蛋白的条件下在生物膜形成中发挥不同作用。方法S. Epidermidis 1585？WT（ICAADBC缺乏），缺乏embp的衍生菌株，从诱导型促进剂表达empp，或从质粒表达ICAADBC，在标准实验室培养基中培养，或用人血浆或血清培养基。量化生物膜的量，结构，弹性和抗微生物渗透，以描述由不同基质组分和生长条件引起的结构差异。最后，我们响应于宿主因子量化悬浮骨料作为悬浮聚合物的发起，以确定细胞响应宿主环境的速度何种速度，并且达到保护它们免受吞噬作用的尺寸。结果S. Epidermidis 1585需要在实验室培养基中形成生物膜的多糖。然而，这些观察结果在人血浆存在下不代表生物膜表型。如果存在人的血浆，对于生物膜形成，多糖和胚胎是多余的。在人血浆中形成的生物膜松散地附着并主要存在于悬浮的聚集体中。在将细胞暴露于血浆或血清的2℃后发生聚集。尽管在不同培养基中产生多糖的生产和胚胎产生菌株形成的生物膜的量和组成的差异，但Vancomycin渗透或易感性没有差异。结论。我们认为，生物膜形成的多糖的假设重要性是从人基质组分的实验室介质中研究生物膜的人工制品。 S.表皮的细胞 - 细胞聚集可以通过宿主因子激活，而不依赖于主要粘附素，PIA和eBP，表明需要重新审视S.PeidermIdis如何部署自我产生的和宿主衍生的矩阵的基本问题组分在体内形成抗生素耐受生物膜。

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