Borrelia outer surface protein C is capable of human fibrinogen binding.
Outer surface protein C (OspC) is one of the most abundant surface lipoproteins produced during early infection by the Borrelia spirochete, the causative agent of Lyme disease. The high sequence variability of the ospC gene results in the production of several and strongly divergent OspC types. One of the known roles of OspC is the recruitment of blood components, including complement regulators, to facilitate the bloodstream survival of Borrelia at an essential stage of host infection. Here, we identify and describe a new interaction between OspC and human fibrinogen. To test the ability of OspC to bind fibrinogen, we developed a microscale thermophoresis assay using four fluorescently labeled types of OspC. We show that OspC binds fibrinogen tightly, with nanomolar Kd, and that the binding depends on the OspC type. The binding assays combined with SAXS studies allowed us to map the OspC-binding site on the fibrinogen molecule. Spectrometric measurements of fibrinogen clotting in the presence of OspC indicate that OspC negatively influences the clot formation process. Taken together, our findings are consistent with the hypothesis that OspC interacts with blood protein partners to facilitate Borrelia spreading by the hematogenous route.
Produced in the liver, fibrinogen is a protein in blood plasma that is essential for the coagulation of blood and is converted to fibrin by the action of thrombin in the presence of ionized calcium. https://medicaldictionary.thefreedictionary.com/fibrinogen. It can become elevated in conditions involving tissue damage, infection, or inflammation. https://link.springer.com/article/10.1007/s00281-011-0290-8.
For a great read on the role fibrin plays in biofilms and cysts: https://www.ppt-health.com/lyme-disease-basics/fibrin-in-biofilms-and-cysts/
This study showed Lyme patients had an increase in fibrinogen: https://bmcinfectdis.biomedcentral.com/articles/10.1186/1471-2334-13-S1-P63
Great article on homocysteine and fibrinogen, two biomarkers of inflammation: http://blog.wellnessfx.com/2013/09/16/take-deeper-look-two-biomarkers-inflammation/ There’s even a link between the two biomarkers. High homocysteine levels block the natural breakdown of fibrinogen, leading to a buildup of fibrinogen in the blood which can cause hyper coagulation.
If you struggle with hyper coagulation (thick blood) work with your practitioner as this can hamper the effectiveness of treatment as well as compromise nutrient and oxygen delivery to the body. Also, thicker blood requires the heart to work harder to circulate blood. Some also feel it can deprive the gut of nourishment and may be a factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. https://www.diagnose-me.com/symptoms-of/hypercoagulation-thickened-blood.php. This link also explains testing as well as potential treatments to discuss with your doctor.
Many Lyme/MSIDS struggle with hyper coagulation. My husband does and took heparin for years during treatment. He felt better immediately. He has since weaned from that onto increased fish oil, Berberine, and Systemic Enzymes. Nattokinase is also recommended.
The take home from this study is that Bb uses components of our blood to propagate itself.