Complement and Thromboinflammation in SARS-CoV-2
When our adaptive immune system fails or responds too slow in pandemics, we need to be able to rely on our host defense and innate immune system. It has not only become more relevant for now, but also for future infections. As within the current SARS-CoV-2 / Covid-19 pandemic it is evident that the innate immune system has a pivotal role in relation to the inflammatory storm in SARS-CoV-2 infected patients. Hyper activation is contributing to lung damage, as well as microvascular injury of the thromboinflammation pathway is observed. We are looking both at the hyperinflammation in which complement appears to play a role, as well as the microvascular endothelial cell injury and pulmonary angioedema in which the kinin pathway plays a role. Hycult Biotech is developing unique reagents as a niche player within Innate Immunity. Our main goal is translating scientific tools into biomarkers for disease activity or validation of biomarkers by actively participating in scientific projects. For this purpose Hycult Biotech engages in a number of recent SARS-CoV-2 initiatives to unravel the inflammatory process and validate biomarkers that are supportive for therapeutic interventions.
|
SARS-CoV-2 studies on complement therapeutics
|
|
|
|
- Kinins and Cytokines in COVID-19: A Comprehensive Pathophysiological Approach
- Thrombomodulin in disseminated intravascular coagulation and other critical conditions-a multi-faceted anticoagulant protein with therapeutic potential
- Soluble Thrombomodulin Increases in Patients with Disseminated Intravascular Coagulation and in Those with Multiple Organ Dysfunction Syndrome after Trauma: Role of Neutrophil Elastase
- Thrombomodulin favors leukocyte microvesicle fibrinolytic activity, reduces NETosis and prevents septic shock-induced coagulopathy in rats
|