Presentation Information
[P04-592]Role of Bacterial Membrane Vesicles in the Pathogenesis of Infective Endocarditis Caused by Streptococcus mutans
○SHI-MIN Hong1, KAI-YANG CHU1, CHIH-CHIEH HSU1 (1. Soochow University (Taiwan))
Keywords:
Bacterial membrane vesicles,Streptococcus mutans,biofilm,infective endocarditis,eDNA
[Purpose]
Bacterial membrane vesicles (MVs) carry cargo that modulates both bacterial and host physiological states, thereby enhancing virulence. Infective endocarditis (IE) is a severe cardiac infection associated with bacterial biofilm formation and is characterized by high mortality and recurrence rates. However, the specific mechanisms by which Streptococcus mutans MVs contribute to IE pathogenesis remain poorly understood.
[Method]
We utilized Nanoparticle Tracking Analysis (NTA) to compare MV profiles between the wild-type and the prsA and atlAmutant strains. Furthermore, in vitro biofilm assays and a catheter-induced rat model of IE were performed to evaluate the impact of these proteins on bacterial virulence and disease progression.
[Results]
Our findings demonstrate that extracellular DNA (eDNA) release is primarily mediated through MV secretion, a process critically dependent on AtlA and PrsA. Notably, exogenous MV supplementation not only restores biofilm formation in atlA and prsA deletion mutants but also significantly enhances bacterial biofilm capacity in IE models. Furthermore, exposure to host plasma triggers robust MV release, thereby fortifying bacterial resistance against immune clearance in human whole blood.
[Consideration]
The presence of essential regulatory and structural proteins within MVs facilitates both biofilm maturation and immune evasion. This underscores vesicle secretion as a key factor in the pathogenic transition of S. mutans from an oral commensal to a systemic pathogen.
[Conclusion]
We identify MVs as indispensable factors in S. mutans virulence during IE progression. Consequently, targeting MV biogenesis or its associated regulatory proteins represents a promising therapeutic strategy for mitigating S. mutans-induced IE.
Bacterial membrane vesicles (MVs) carry cargo that modulates both bacterial and host physiological states, thereby enhancing virulence. Infective endocarditis (IE) is a severe cardiac infection associated with bacterial biofilm formation and is characterized by high mortality and recurrence rates. However, the specific mechanisms by which Streptococcus mutans MVs contribute to IE pathogenesis remain poorly understood.
[Method]
We utilized Nanoparticle Tracking Analysis (NTA) to compare MV profiles between the wild-type and the prsA and atlAmutant strains. Furthermore, in vitro biofilm assays and a catheter-induced rat model of IE were performed to evaluate the impact of these proteins on bacterial virulence and disease progression.
[Results]
Our findings demonstrate that extracellular DNA (eDNA) release is primarily mediated through MV secretion, a process critically dependent on AtlA and PrsA. Notably, exogenous MV supplementation not only restores biofilm formation in atlA and prsA deletion mutants but also significantly enhances bacterial biofilm capacity in IE models. Furthermore, exposure to host plasma triggers robust MV release, thereby fortifying bacterial resistance against immune clearance in human whole blood.
[Consideration]
The presence of essential regulatory and structural proteins within MVs facilitates both biofilm maturation and immune evasion. This underscores vesicle secretion as a key factor in the pathogenic transition of S. mutans from an oral commensal to a systemic pathogen.
[Conclusion]
We identify MVs as indispensable factors in S. mutans virulence during IE progression. Consequently, targeting MV biogenesis or its associated regulatory proteins represents a promising therapeutic strategy for mitigating S. mutans-induced IE.
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