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The two-component system VicRK regulates functions associated with Streptococcus mutans resistance to complement
Livia A Alves1, Erika N Harth-Chu1, Thais H Palma1
1Department of Oral Diagnosis, Piracicaba Dental School - State University of Campinas, Piracicaba, SP, Brazil.
Molecular Oral Microbiology
|April 7, 2017
Summary
Streptococcus mutans uses peptidases to evade the immune system, a process regulated by the VicRK two-component system. This mechanism helps the bacteria survive in the bloodstream and cause systemic infections.
Area of Science:
- Microbiology
- Immunology
- Molecular Biology
Background:
- Streptococcus mutans causes dental caries and can lead to systemic infections.
- The two-component system (TCS) VicRKSm regulates virulence factors in S. mutans.
- Understanding S. mutans' interaction with host immunity is crucial for combating infections.
Purpose of the Study:
- To investigate how the VicRKSm TCS influences S. mutans' susceptibility to blood-mediated immunity.
- To identify specific genes and mechanisms involved in complement evasion.
Main Methods:
- Comparative analysis of wild-type and vicKSm mutant strains of S. mutans.
- Assessment of complement C3b deposition, IgG binding, and opsonophagocytosis.
- Gene expression analysis using reverse transcriptase quantitative polymerase chain reaction (RT-qPCR).
- Gene deletion studies to confirm the role of specific peptidases.
Main Results:
- The vicKSm mutant showed reduced C3b deposition, IgG binding, and opsonophagocytosis.
- Genes encoding peptidases (pepO and smu.399) were upregulated in the mutant in serum.
- Deletion of pepO and smu.399 enhanced C3b deposition and opsonophagocytosis.
- The mutant exhibited increased fibronectin binding but impaired ex vivo blood persistence due to growth defects.
Conclusions:
- S. mutans utilizes peptidase-mediated mechanisms for complement evasion, controlled by the VicRKSm TCS.
- These peptidases play a significant role in resisting blood-mediated immunity.
- While immune evasion is enhanced, bacterial persistence in blood is limited by other factors like growth defects.