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Streptococcal collagen-like protein 1, Scl1, modulates group a Streptococcus adhesion, biofilm formation and virulence

机译：链球菌胶原蛋白样蛋白1，Scl1，调节a组链球菌的粘附，生物膜形成和毒力

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摘要

Background: The collagens comprise a large family of versatile proteins found in all three domains of life. The streptococcal collagen-like protein 1, scl1, of group A Streptococcus (GAS) binds extracellular matrix components (ECM), cellular fibronectin and laminin, via the surface-exposed globular domain. GAS strains express scl1 and form biofilm in vitro, except for M3-type strains that are particularly invasive to humans. Hypothesis: Lack of scl1 adhesin in M3 GAS results in decreased adherence and biofilm formation, and increased virulence. Results and Discussion : First crystal structure of the globular domain revealed a unique six-helical bundle fold, consisting of three pairs of alpha helices connected by variable loops. ECM binding by Scl1 promotes the formation of stable tissue microcolonies, which was demonstrated in vitro during infection of wounded human skin equivalents. A conserved nonsense mutation was identified in the scl1 allele of the M3-type strains (scl1.3) that truncates the coding sequence, presumably resulting in a secreted Scl1 variant. Absence of Scl1 on the surface of M3-type GAS was demonstrated experimentally, as well as diminished expression of the scl1 transcript in M3 strains relative to other M-types. Therefore, M3-type strains have reduced biofilm capacity on ECM coatings relative to other M-types. Constructed full-length recombinant Scl1.3 protein displayed binding capacity to cellular fibronectin and laminin, and M3 strains complemented with functional Scl1.3 adhesin displayed increased biofilm formation. The isoallelic M3 strain, carrying a rare "carrier" allele encoding cell-associated Scl1.3 variant, showed decreased pathology in mice, compared to the invasive M3 strain. Similarly, scl1 inactivation in biofilm-capable M28- and M41-type GAS led to increased lesion size during subcutaneous infection. Conclusions: The studies presented here demonstrate the importance of surface Scl1 in modulating biofilm formation and virulence of GAS, and provide insight into the structure and function of Scl proteins.
机译：背景：胶原蛋白包含在生命的所有三个域中发现的大量通用蛋白家族。 A组链球菌（GAS）的链球菌胶原蛋白样蛋白1（scl1）通过表面暴露的球状结构域结合细胞外基质成分（ECM），细胞纤连蛋白和层粘连蛋白。 GAS菌株在体外表达scl1并形成生物膜，但对人类特别具有侵害性的M3型菌株除外。假设：M3 GAS中缺少scl1粘附素会导致粘附和生物膜形成减少，并增加毒力。结果与讨论：球形域的第一个晶体结构显示出独特的六螺旋束折叠，由三对由可变环连接的α螺旋组成。通过Scl1的ECM结合促进了稳定的组织微菌落的形成，这在受伤的人类皮肤等效物的感染过程中得到了体外证明。在M3型菌株（scl1.3）的scl1等位基因中鉴定了保守的无义突变，该突变截短了编码序列，推测是导致分泌的Scl1变体。实验证明了M3型GAS表面上Scl1的缺失，以及相对于其他M型，M3菌株中scl1转录物的表达减少。因此，相对于其他M型，M3型菌株在ECM涂层上的生物膜容量降低。构建的全长重组Scl1.3蛋白表现出与细胞纤连蛋白和层粘连蛋白的结合能力，并且补充有功能性Scl1.3粘附素的M3菌株表现出增加的生物膜形成。与侵袭性M3菌株相比，携带罕见的“携带者”等位基因编码细胞相关Scl1.3变体的等位基因M3菌株在小鼠中的病理学降低。同样，具有生物膜功能的M28和M41型GAS中的scl1失活导致皮下感染期间病变大小的增加。结论：这里提出的研究证明表面Scl1在调节GAS的生物膜形成和毒力中的重要性，并提供对Scl蛋白的结构和功能的了解。

著录项

  • 作者

    Bachert, Beth Alexandra.;

  • 作者单位

    West Virginia University.;

  • 授予单位 West Virginia University.;
  • 学科 Microbiology.;Virology.
  • 学位 Ph.D.
  • 年度 2016
  • 页码 307 p.
  • 总页数 307
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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