Two distinct pathways for the invasion of Streptococcus pyogenes in non-phagocytic cells
Two distinct pathways for the invasion of Streptococcus pyogenes in non-phagocytic cells
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DOI：
10.1046/j.1462-5822.2000.00040.x
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发表时间：
2000-04-01
影响因子：
3.4
通讯作者：
Chhatwal, GS
中科院分区：
文献类型：
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作者：
Molinari, G;Rohde, M;Chhatwal, GS
上皮细胞的粘附和侵袭是化脓性链球菌的重要致病机制。S.化脓性链球菌SfbI蛋白参与粘附和侵袭过程。含SfbI菌株的侵入被怀疑是抗生素治疗未能根除S.化脓在这项研究中，我们测试了两个良好的特点的临床分离株：A40，表达SfbI和A8，这是SfbI阴性，不能结合纤连蛋白的粘附和侵袭特性。在菌株A40中，SfbI是通过使用纤连蛋白作为桥接分子和α（5）β（1）整联蛋白作为细胞受体而附着和侵袭所需的主要因子。摄取过程的特点是在细菌-细胞界面产生大的膜内陷，没有肌动蛋白募集或细胞损伤的证据。A40细胞位于吞噬体中，并且在感染后仅24小时，细菌群体的一致部分到达细胞质。与此相反，吸收菌株A8需要主要的细胞骨架蛋白下面附着的细菌重排。在A8中，涉及蛋白质部分，其不与α（5）β（1）相互作用或不需要任何已知的桥接分子。细菌附着刺激邻近微绒毛的伸长和大量募集，微绒毛融合到链球菌链周围。它们导致了大型伪足状结构的产生，这些结构吞噬了在细胞质中快速释放和复制的细菌。本文报道的两种完全不同的摄取途径的鉴定为S.化脓性链球菌的分离，并可能有助于了解致病机制和持久性的S。化脓
Adherence to and invasion of epithelial cells represent important pathogenic mechanisms of Streptococcus pyogenes. A fibronectin-binding surface protein of S. pyogenes, SfbI protein, has been implicated in both adherence and invasion processes. Invasion of SfbI-containing strains has been suspected to be responsible for the failure of antibiotics treatment to eradicate S. pyogenes. In this study, we tested the adherence and invasion properties of two well-characterized clinical isolates: A40, which expresses SfbI; and A8, which is SfbI negative and is unable to bind fibronectin. In strain A40, SfbI was the main factor required for attachment and invasion by using fibronectin as a bridging molecule and the alpha(5)beta(1) integrin as cellular receptor. The uptake process was characterized by the generation of large membrane invaginations at the bacteria-cell interface without evidence of actin recruitment or cellular injury. A40 cells were located in phagosomes and, only 24 h after infection, a consistent part of the bacterial population reached the cytoplasm. In contrast, uptake of strain A8 required major rearrangements of cytoskeletal proteins underneath attached bacteria. In A8, a proteinaceous moiety was involved, which does not interact with alpha(5)beta(1) or need any known bridging molecule. Bacterial attachment stimulated elongation and massive recruitment of neighbouring microvilli, which fused to surround streptococcal chains. They led to the generation of large pseudopod-like structures, which engulfed bacteria that were rapidly released and replicated in the cytoplasm. The identification of two completely different uptake pathways reported here provided further evidence regarding the diversity of S. pyogenes isolates and might contribute towards understanding the pathogenesis and persistence of S. pyogenes.