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Human transferrin as a source of iron for Streptococcus intermedius
V Brochu1, D Greinier, D Mayrand
1Groupe de Recherche en Ecologie Buccale, Faculté de Médecine Dentaire, Université Laval, Québec, Canada.
FEMS Microbiology Letters
|September 19, 1998
Summary
Streptococcus intermedius bacteria can cause severe infections by obtaining iron from human transferrin. This occurs by lowering the pH of the surrounding environment, releasing iron for bacterial growth.
Area of Science:
- Microbiology
- Infectious Diseases
- Bacterial Pathogenesis
Background:
- Streptococcus intermedius is a known pathogen causing severe infections.
- Understanding how bacteria acquire essential nutrients like iron is crucial for explaining pathogenesis.
Purpose of the Study:
- To investigate the mechanism by which Streptococcus intermedius utilizes human transferrin as an iron source.
- To identify the specific pathways involved in iron acquisition from transferrin by S. intermedius.
Main Methods:
- Cultivating S. intermedius in iron-deficient media supplemented with iron sources (ferrous sulfate, holotransferrin).
- Analyzing bacterial growth and gene expression under iron-limited conditions.
- Assessing siderophore, reductase, transferrin-binding, and proteolytic activities.
- Monitoring and manipulating the pH of the culture medium.
Main Results:
- S. intermedius growth was supported by ferrous sulfate and holotransferrin in iron-deficient media.
- Iron-poor conditions led to the overexpression of a 58 kDa cell surface protein.
- No siderophore, reductase, transferrin-binding, or proteolytic activity was detected.
- S. intermedius rapidly lowered the medium pH, releasing iron from holotransferrin.
- Increased buffering capacity inhibited growth, indicating pH-dependent iron release.
Conclusions:
- Streptococcus intermedius acquires iron from transferrin primarily by acidifying the surrounding environment.
- This pH-lowering mechanism facilitates iron release from holotransferrin, supporting bacterial growth.
- The findings suggest a novel mechanism for S. intermedius pathogenesis, involving localized environmental modification.