当前位置: X-MOL 学术Arch. Microbiol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Characterization and pathogenicity of fibronectin binding protein FbpI of Streptococcus intermedius
Archives of Microbiology ( IF 2.8 ) Pub Date : 2020-06-01 , DOI: 10.1007/s00203-020-01922-y
Yoshitoyo Kodama 1 , Yu Shimoyama 1 , Taichi Ishikawa 1 , Shigenobu Kimura 1 , Minoru Sasaki 1
Affiliation  

Streptococcus intermedius is a causative agent of brain or liver abscesses. S. intermedius produces intermedilysin that plays a pivotal role in pathogenicity. We identified other pathogenic factors and described a fibronectin binding protein (FBP) homolog of S. intermedius (FbpI) that mediated bacterial adhesion to epithelial cells and virulence for mice. The amino acid sequence of FbpI is similar to that of atypical FBPs, which do not possess a conventional secretion signal and an anchoring motif. A full-length recombinant FbpI (rFbpI) bound to immobilized fibronectin in a dose-dependent manner. The fibronectin binding activity of an N-terminal construct of rFbpI comprising the translation initiation methionine of the open reading frame to lysine 265 (rFbpI-N) bound immobilized fibronectin to a much lesser extent compared with rFbpI. A construct comprising the C-terminal domain (alanine 266 to methionine 549; rFbpI-C) bound immobilized fibronectin equivalently to rFbpI. Adherence of the isogenic mutant ΔfbpI to cultured epithelial cells and immobilized fibronectin was significantly lower than that of the wild-type strain. Abscess formation of ΔfbpI reduced in a mouse infection model compared with that in the wild-type. Thus, FbpI may play a role in bacterial adhesion to host cells and represent a critical pathogenic factor of S. intermedius.

中文翻译:

中间链球菌纤连蛋白结合蛋白 FbpI 的表征和致病性

中间链球菌是脑或肝脓肿的病原体。S. intermedius 产生在致病性中起关键作用的中间溶素。我们确定了其他致病因素,并描述了中间链球菌 (FbpI) 的纤连蛋白结合蛋白 (FBP) 同源物,其介导细菌与上皮细胞的粘附和小鼠的毒力。FbpI 的氨基酸序列与不具有常规分泌信号和锚定基序的非典型 FBP 的氨基酸序列相似。全长重组 FbpI (rFbpI) 以剂量依赖性方式与固定化纤连蛋白结合。与 rFbpI 相比,包含开放阅读框的翻译起始甲硫氨酸到赖氨酸 265 (rFbpI-N) 的 rFbpI 的 N 端构建体的纤连蛋白结合活性结合固定化纤连蛋白的程度要小得多。包含C-末端结构域(丙氨酸266至甲硫氨酸549;rFbpI-C)的构建体与rFbpI等效地结合固定化纤连蛋白。同基因突变体 ΔfbpI 对培养的上皮细胞和固定化纤连蛋白的粘附显着低于野生型菌株。与野生型相比,小鼠感染模型中 ΔfbpI 的脓肿形成减少。因此,FbpI 可能在细菌与宿主细胞的粘附中发挥作用,并代表中间链球菌的关键致病因素。与野生型相比,小鼠感染模型中 ΔfbpI 的脓肿形成减少。因此,FbpI 可能在细菌与宿主细胞的粘附中发挥作用,并代表中间链球菌的关键致病因素。与野生型相比,小鼠感染模型中 ΔfbpI 的脓肿形成减少。因此,FbpI 可能在细菌与宿主细胞的粘附中发挥作用,并代表中间链球菌的关键致病因素。
更新日期:2020-06-01
down
wechat
bug