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In vivo binding of complement regulator factor H by Streptococcus pneumoniae
Lisa R Quin1, Stephanie Carmicle, Sandhya Dave
1Department of Microbiology, University of Mississippi Medical Center, Jackson, MS 39216, USA.
The Journal of Infectious Diseases
|November 4, 2005
Summary
Pneumococcal surface protein C (PspC) binds to factor H (FH), enhancing bacterial proliferation and virulence. This interaction was observed in vivo, with higher FH binding and PspC expression following intraperitoneal infection in mice.
Area of Science:
- Microbiology
- Immunology
- Molecular Biology
Background:
- Pneumococcal surface protein C (PspC) interacts with factor H (FH), a complement regulator.
- FH binding to PspC inhibits the alternative complement pathway.
Purpose of the Study:
- To investigate the in vivo interaction between FH and pneumococci during systemic infection.
- To determine the effect of FH binding on pneumococcal PspC expression and proliferation.
Main Methods:
- Mouse model of systemic infection (intraperitoneal and intravenous challenge).
- Flow-cytometric analysis to quantify FH and PspC binding.
- Real-time PCR to measure PspC mRNA levels.
Main Results:
- FH binding to pneumococci was higher after intraperitoneal challenge compared to intravenous challenge.
- PspC mRNA levels and expression were significantly upregulated following intraperitoneal infection.
- Pneumococci pre-bound with FH exhibited increased proliferation in vivo.
Conclusions:
- The interaction between PspC and FH contributes to pneumococcal virulence.
- FH binding enhances pneumococcal survival and proliferation during infection.