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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.
Abstract:
Pneumococcal surface protein C (PspC) binds to the complement regulatory protein factor H (FH), which inhibits alternative pathway activation. In the present study, using a mouse model of systemic infection and flow-cytometric analyses, we demonstrated an in vivo interaction between FH and pneumococci and showed differential FH binding during bacteremia. Flow-cytometric analyses of pneumococci harvested after intraperitoneal (ip) challenge demonstrated increased binding of FH, compared with that after intravenous (iv) challenge. Real-time polymerase chain reaction analyses of PspC mRNA showed that, relative to pneumococci grown in vitro, those recovered from the blood of mice 24 h after iv challenge exhibited 23-fold higher mRNA levels; however, after ip challenge, PspC mRNA induction was increased 870-fold. A subsequent increase in PspC expression was detected by flow cytometry using a monoclonal antibody against PspC. Furthermore, pneumococci with FH bound to complement before exposure had increased proliferation, compared with pneumococci not pretreated with FH. These results suggest that the interaction between PspC and FH contributes to pneumococcal virulence.
Insights
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.
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