Posted by Adam Awdish on
Human Factor II (Prothrombin) Purified, Human Fibrinogen Purified, and Rabbit Anti Mouse/Rat Fibrinogen Polyclonal Affinity Purified from Innovative Research were used in the following study:
Alice G. Cheng, Molly McAdow, Hwan K. Kim, Taeok Bae, Dominique M. Missiakas, Olaf Schneewind
August 5, 2010
Staphylococcus aureus is a bacterium responsible for many common infections, including bacteremia, pneumonia, soft tissue infections, and septic arthritis among others. There remains no known way to gain protective immunity against S. aureus diseases, and researchers continue to investigate options for an effective vaccine.
Once S. aureus enters a host’s bloodstream, depending on the strain of S. aureus, it disseminates into various tissues in the body. From there it seeds abscesses that grow and eventually rupture, providing the pathogen the opportunity to enter circulation and spread to uninfected tissues.
Researchers in this study tested various secreted proteins to explore options for a vaccine candidate to protect against S. aureus. They had a particular focus on Coagulase (Coa), which is secreted by virtually all isolates of S. aureus.
During infection of the host, Coa activates prothrombin, causing the cleavage of fibrinogen to fibrin. The Coa-prothrombin complexes are not targeted by thrombin inhibitors, allowing Coa to skip regulatory steps in blood coagulation pathways. This makes the binding of S. aureus to prothrombin an important component of S. aureus driven pathogenesis.
S. aureus also secretes von Willebrand factor-binding protein (vWbp). This secondary coagulase, the amino acid structure of which exhibits similarities to Coa, also promotes cleavage of fibrinogen to fibrin due to its ability to associate with prothrombin. Previous studies have observed that vWbp is preferential towards activation of human prothrombin, while Coa coagulase is indiscriminate between human, rabbit, and mouse with regard to clotting plasma.
Here, researchers examined samples of kidney tissue from hosts infected with S. aureus and used histochemical staining to identify prothrombin and fibrinogen/fibrin within the abscesses that form during infection. Furthermore, the study results support that both Coa and vWbp contribute to the survival and pathogenesis of S. aureus. When both Coa and vWbp are present, they promote non-proteolytic activation of prothrombin as well as the cleavage of fibrinogen. Further testing revealed that antibodies that target Coa or vWbp can reduce their ability to bind to prothrombin and form active complexes which then act on fibrinogen. These results suggest that further study and development of vaccines that target Coa and vWbp as antigens may find efficacy against S. aureus infections.
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