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Cultivation Methods of Spirochetes from Borrelia burgdorferi Sensu Lato Complex and Relapsing Fever Borrelia
Published on: November 25, 2022
CspA from Borrelia burgdorferi inhibits the terminal complement pathway
Teresia Hallström1, Corinna Siegel, Matthias Mörgelin
1Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, Hans Knöll Institute, Jena, Germany.
Mbio
|August 15, 2013
Summary
Borrelia burgdorferi uses CspA to block the terminal complement pathway, inhibiting terminal complement complex assembly and insertion. This mechanism allows the bacteria to survive in human serum.
Area of Science:
- Microbiology
- Immunology
- Biochemistry
Background:
- Borrelia burgdorferi evades the human immune system by controlling complement activation.
- The bacterium utilizes immune evasion proteins like CspA to bind human plasma regulators.
- Previous research suggested CspA might have additional immune control functions.
Purpose of the Study:
- To identify new mechanisms of Borrelia burgdorferi immune evasion.
- To investigate the role of CspA in controlling the terminal complement pathway.
- To determine if CspA inhibits terminal complement complex (TCC) assembly and function.
Main Methods:
- Hemolytic assays were used to assess CspA's effect on TCC assembly.
- CspA's binding to human terminal complement components C7 and C9 was analyzed.
- CspA was ectopically expressed on Borrelia garinii to test for serum resistance.
Main Results:
- CspA was identified as a direct inhibitor of the terminal complement pathway.
- CspA binds to human C7 and C9, blocking TCC assembly and membrane insertion.
- Ectopic expression of CspA conferred serum resistance to Borrelia garinii by inhibiting TCC assembly.
- CspA inhibits TCC assembly at the C7 level and prevents C9 polymerization.
Conclusions:
- CspA is a novel bacterial inhibitor of the terminal complement pathway.
- CspA's ability to block TCC assembly is crucial for Borrelia burgdorferi survival in human serum.
- CspA represents a potential biomarker and therapeutic target for borrelial infections.
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