Staphylococcus epidermidis Uses Distinct Mechanisms of Biofilm Formation To Interfere with Phagocytosis and Activation of Mouse Macrophage-Like Cells 774A.1
Staphylococcus epidermidis Uses Distinct Mechanisms of Biofilm Formation To Interfere with Phagocytosis and Activation of Mouse Macrophage-Like Cells 774A.1
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DOI：
10.1128/iai.01142-10
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发表时间：
2011-06-01
影响因子：
3.1
通讯作者：
Rohde, Holger
中科院分区：
文献类型：
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作者：
Schommer, Nina N.;Christner, Martin;Rohde, Holger
粘附生物膜的组装是设备相关感染期间表皮葡萄球菌毒力的关键机制。除了多糖细胞间粘附素（PIA）外，积累相关蛋白 Aap 和细胞外基质结合蛋白 Embp 也充当细胞间粘附素，介导表皮葡萄球菌细胞聚集和生物膜积累。本研究的目的是更详细地研究 PIA、Aap 和 Embp 介导的表皮葡萄球菌生物膜的结构特征，并评估它们对生物膜相关表皮葡萄球菌免疫逃逸的具体贡献。 PIA、Embp 和 Aap 介导的生物膜表现出显着的形态差异。基本上，PIA 合成诱导肉眼可见的粗糙细胞簇的形成，而 Aap 和 Embp 依赖性生物膜优先显示聚集细菌的光滑层。在微观水平上，PIA被发现形成连接细菌的线状有组织的细胞外基质，而Embp产生细胞间基质的小沉积物，而Aap严格定位于细菌表面。尽管存在显着差异，但使用 PIA、Aap 或 Embp 形成生物膜的表皮葡萄球菌菌株可免受 J774A.1 巨噬细胞的摄取，且具有相似的效率。此外，与生物膜阴性表皮葡萄球菌菌株相比，同基因生物膜形成表皮葡萄球菌仅诱导炎症 J774A.1 巨噬细胞反应减弱，导致 NF-κ B 激活显着降低（88.2% 至 88.7%），白细胞介素 1 β (IL-1 β) 产生显着降低 68.8% 至 83%。尽管细菌细胞表面仍然装饰着各自的细胞间粘附素，但机械生物膜分散部分恢复了 NF-κ B 激活的诱导。我们的结果表明，不同的表皮葡萄球菌生物膜形态类型在保护表皮葡萄球菌免遭吞噬细胞摄取和对抗巨噬细胞活化方面同样有效，为可能导致生物膜相关表皮葡萄球菌异物感染慢性和持续过程的机制提供了新的见解。
Assembly of adherent biofilms is the key mechanism involved in Staphylococcus epidermidis virulence during device-associated infections. Aside from polysaccharide intercellular adhesin (PIA), the accumulation-associated protein Aap and the extracellular matrix binding protein Embp act as intercellular adhesins, mediating S. epidermidis cell aggregation and biofilm accumulation. The aim of this study was to investigate structural features of PIA-, Aap-, and Embp-mediated S. epidermidis biofilms in more detail and to evaluate their specific contributions to biofilm-related S. epidermidis immune escape. PIA-, Embp-, and Aap-mediated biofilms exhibited substantial morphological differences. Basically, PIA synthesis induced formation of macroscopically visible, rough cell clusters, whereas Aap- and Embp-dependent biofilms preferentially displayed a smooth layer of aggregated bacteria. On the microscopic level, PIA was found to form a string-like organized extracellular matrix connecting the bacteria, while Embp produced small deposits of intercellular matrix and Aap was strictly localized to the bacterial surface. Despite marked differences, S. epidermidis strains using PIA, Aap, or Embp for biofilm formation were protected from uptake by J774A.1 macrophages, with similarly efficiencies. In addition, compared to biofilm-negative S. epidermidis strains, isogenic biofilm-forming S. epidermidis induced only a diminished inflammatory J774A.1 macrophage response, leading to significantly (88.2 to 88.7%) reduced NF-kappa B activation and 68.8 to 83% reduced interleukin-1 beta (IL-1 beta) production. Mechanical biofilm dispersal partially restored induction of NF-kappa B activation, although bacterial cell surfaces remained decorated with the respective intercellular adhesins. Our results demonstrate that distinct S. epidermidis biofilm morphotypes are similarly effective at protecting S. epidermidis from phagocytic uptake and at counteracting macrophage activation, providing novel insights into mechanisms that could contribute to the chronic and persistent course of biofilm-related S. epidermidis foreign material infections.