Pathogenesis of Campylobacter fetus infections. Role of surface array proteins in virulence in a mouse model
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Summary
This summary is machine-generated.The surface array protein (S-protein) capsule significantly increases Campylobacter fetus virulence in mice. This S-protein enhances bacterial survival and causes higher mortality, highlighting its key role in infection pathogenesis.
Area Of Science
- Microbiology
- Infectious Diseases
- Bacterial Pathogenesis
Background
- Campylobacter fetus is a significant bacterial pathogen.
- The role of surface array protein (S-protein) capsules in C. fetus virulence is not fully understood.
- Existing models do not adequately explain the S-protein's contribution to pathogenesis.
Purpose Of The Study
- To develop and utilize a mouse model to compare the virulence of S-protein-positive (S-plus) and S-protein-negative (S-minus) C. fetus strains.
- To elucidate the specific role of the S-protein capsule in C. fetus infection and disease progression.
Main Methods
- Generation of a mouse model using HA/ICR mice pretreated with ferric chloride.
- Oral challenge experiments with S-plus and S-minus C. fetus strains and their mutants.
- Assessment of virulence via LD50 determination, mortality rates, and bacteremia levels.
- In vivo experiments using S-protein antiserum and free S-proteins to evaluate S-protein's direct impact.
Main Results
- The S-plus strain exhibited significantly lower LD50 (43.3-fold) compared to its S-minus mutant.
- High-grade bacteremia was observed with S-plus strains but not with S-minus strains.
- Mice pretreated with anti-S-protein antiserum showed a 51.6-fold reduction in bacteremia.
- Challenge with S-minus strain and free S-proteins resulted in 30% mortality, indicating S-protein's role in virulence.
Conclusions
- The S-protein capsule is a critical virulence factor for Campylobacter fetus.
- S-protein enhances bacterial survival and promotes high-grade bacteremia, leading to increased mortality.
- The S-protein is not inherently toxic but significantly contributes to pathogenesis when present on the bacterial surface.