Presentation Information
[P04-603]The Type VII Secretion System is Essential for Immune Evasion and Biofilm Maturation in Streptococcus gordonii-Induced IE
○KAI-YANG CHU1, SHIN-MIN HONG1, CHIH-CHIEH HSU1 (1. Soochow University, Taipei, Taiwan(Taiwan) (Taiwan))
Keywords:
Infective endocarditis,Streptococcus gordonii,The Type VII secretion system
[Purpose]
Infective endocarditis (IE) is a cardiovascular disease characterized by a high recurrence rate and high mortality. Although Streptococcus gordonii is a normal commensal in the oral cavity, it is a major pathogen causing endocarditis. The Type VII secretion system was first discovered in Gram-positive bacteria and has been shown to regulate the virulence of various bacteria, but its specific role in IE caused by S. gordonii remains unclear.
[Method]
A T7SS-deficient mutant was constructed using an allelic replacement strategy and confirmed via DNA sequencing. The impact of T7SS on biofilm formation was evaluated using a static microtiter plate assay with crystal violet staining. Furthermore, a catheter-induced rat model of IE was employed to assess in vivo virulence.
[Results]
Genomic analysis revealed that S. gordonii can be divided into two distinct groups based on EssC polymorphism, with clinical isolates showing significant differences in their endocarditis-inducing capacity. Functional assays demonstrated that the loss of T7SS components significantly impaired bacterial survival in the bloodstream and reduced the ability to cause IE. Mechanistically, these mutants exhibited a diminished capacity to release eDNA and form stable biofilms with platelets. Notably, the deletion of effectors esxA and sgo0065 to sgO0070 led to a reduced ability to lyse red blood cell and neutrophils, directly correlating with decreased in vivo survival and attenuated infectivity.
[Consideration]
This study demonstrates that the T7SS coordinates biofilm formation and immune evasion through EssC, establishing the T7SS as a critical factor for the transition of S. gordonii from an oral commensal to a potent agent of IE.
[Conclusion]
Our findings identify EssC as a key marker for strain-specific virulence and demonstrate that the T7SS, through its effector proteins, is essential for immune evasion, cytolytic activity, and biofilm formation. These results highlight the T7SS as a critical virulence determinant in the development of S. gordonii-induced IE.
Infective endocarditis (IE) is a cardiovascular disease characterized by a high recurrence rate and high mortality. Although Streptococcus gordonii is a normal commensal in the oral cavity, it is a major pathogen causing endocarditis. The Type VII secretion system was first discovered in Gram-positive bacteria and has been shown to regulate the virulence of various bacteria, but its specific role in IE caused by S. gordonii remains unclear.
[Method]
A T7SS-deficient mutant was constructed using an allelic replacement strategy and confirmed via DNA sequencing. The impact of T7SS on biofilm formation was evaluated using a static microtiter plate assay with crystal violet staining. Furthermore, a catheter-induced rat model of IE was employed to assess in vivo virulence.
[Results]
Genomic analysis revealed that S. gordonii can be divided into two distinct groups based on EssC polymorphism, with clinical isolates showing significant differences in their endocarditis-inducing capacity. Functional assays demonstrated that the loss of T7SS components significantly impaired bacterial survival in the bloodstream and reduced the ability to cause IE. Mechanistically, these mutants exhibited a diminished capacity to release eDNA and form stable biofilms with platelets. Notably, the deletion of effectors esxA and sgo0065 to sgO0070 led to a reduced ability to lyse red blood cell and neutrophils, directly correlating with decreased in vivo survival and attenuated infectivity.
[Consideration]
This study demonstrates that the T7SS coordinates biofilm formation and immune evasion through EssC, establishing the T7SS as a critical factor for the transition of S. gordonii from an oral commensal to a potent agent of IE.
[Conclusion]
Our findings identify EssC as a key marker for strain-specific virulence and demonstrate that the T7SS, through its effector proteins, is essential for immune evasion, cytolytic activity, and biofilm formation. These results highlight the T7SS as a critical virulence determinant in the development of S. gordonii-induced IE.
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