Streptococcus mutans PrsA mediates AtlA secretion contributing to extracellular DNA release and biofilm formation in the pathogenesis of infective endocarditis
Chih-Chieh Hsu,
Ron-Bin Hsu,
Xoong-Harng Oon,
Ya-Tang Chen,
Jeng-Wei Chen,
Che-Hao Hsu,
Yu-Min Kuo,
Yi-Hsien Shih,
Jean-San Chia,
Chiau-Jing Jung
Affiliations
Chih-Chieh Hsu
Graduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan
Ron-Bin Hsu
Department of Surgery, Division of Cardiovascular Surgery, National Taiwan University Hospital , College of Medicine, National Taiwan University, Taipei, Taiwan
Xoong-Harng Oon
Graduate Institute of Medical Sciences, College of Medicine, Taipei medical University, Taipei, Taiwan
Ya-Tang Chen
Graduate Institute of Medical Sciences, College of Medicine, Taipei medical University, Taipei, Taiwan
Jeng-Wei Chen
Department of Surgery, Division of Cardiovascular Surgery, National Taiwan University Hospital , College of Medicine, National Taiwan University, Taipei, Taiwan
Che-Hao Hsu
Graduate Institute of Medical Sciences, College of Medicine, Taipei medical University, Taipei, Taiwan
Yu-Min Kuo
Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan
Yi-Hsien Shih
Department of Dermatology, Taipei Medical University-Shuang Ho Hospital, New Taipei City, Taiwan
Jean-San Chia
Graduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan
Chiau-Jing Jung
Graduate Institute of Medical Sciences, College of Medicine, Taipei medical University, Taipei, Taiwan
The role of secretion chaperone-regulated virulence proteins in the pathogenesis of infective endocarditis (IE) induced by viridans streptococci such as Streptococcus mutans 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 S. mutans-induced IE. We found that a prsA-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 in vitro was reduced in the prsA-deficient mutant strain, and complementation of recombinant AtlA in the culture medium restored a wild type biofilm phenotype of the prsA-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 S. mutans PrsA could regulate AtlA-mediated eDNA release to contribute to biofilm formation in the pathogenesis of IE.
