Graduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan.
Graduate Institute of Oral Biology, School of Dentistry, National Taiwan University, Taipei, Taiwan.
Virulence. 2022 Dec;13(1):1379-1392. doi: 10.1080/21505594.2022.2105351.
The role of secretion chaperone-regulated virulence proteins in the pathogenesis of infective endocarditis (IE) induced by viridans streptococci such as is unclear. In this study, we investigated the contribution of the foldase protein PrsA, a putative parvulin-type peptidyl-prolyl isomerase, to the pathogenesis of -induced IE. We found that a -deficient strain had reduced virulence in terms of formation of vegetation on damaged heart valves, as well as reduced autolysis activity, eDNA release and biofilm formation capacity. The secretion and surface exposure of AtlA was reduced in the -deficient mutant strain, and complementation of recombinant AtlA in the culture medium restored a wild type biofilm phenotype of the -deficient mutant strain. This result suggests that secretion and surface localization of AtlA is regulated by PrsA during biofilm formation. Together, these results demonstrate that PrsA could regulate AtlA-mediated eDNA release to contribute to biofilm formation in the pathogenesis of IE.
卷曲相关毒力蛋白在草绿色链球菌（如 ）引起的感染性心内膜炎（IE）发病机制中的作用尚不清楚。在这项研究中，我们研究了折叠酶蛋白 PrsA（一种假定的 parvulin 型肽基脯氨酰顺反异构酶）对 -诱导 IE 发病机制的贡献。我们发现， -缺陷菌株在受损心瓣膜上形成植被、自溶活性、eDNA 释放和生物膜形成能力方面的毒力降低。在 -缺陷突变菌株中，AtlA 的分泌和表面暴露减少，而在培养基中补充重组 AtlA 则恢复了 -缺陷突变菌株的野生型生物膜表型。这一结果表明，在生物膜形成过程中，AtlA 的分泌和表面定位受到 PrsA 的调节。综上所述，这些结果表明 PrsA 可以调节 AtlA 介导的 eDNA 释放，从而有助于 IE 发病机制中的生物膜形成。
