Thrombotic and microvascular complications are a major driver of severe COVID-19. During an acute SARS-CoV-2 infection, patients can experience venous thrombotic events (such as pulmonary embolism) accompanied by elevated D-dimer levels and systemic disease. Currently, there is little mechanistic understanding of how SARS-CoV-2 infection drives such vascular dysfunction in both acute and long COVID, and thus therapeutic approaches to prevent or treat these vascular complications are limited. It is known that patients with acute, severe COVID-19 exhibit a sustained inflammatory response. Multiple studies attribute this sustained inflammatory response to both the infected epithelium and to myeloid cells, wherein macrophage activation, monocyte NLRP3 inflammasome signalling, complement activation and extrusion of neutrophil extracellular traps are implicated.
Dr Gordon’s research focuses on determining the underlying cause of endothelial cell dysfunction in COVID-19. They have found that vascular endothelial cells respond to an adjacent epithelial cell infection, suggesting that the inflammatory micro-environment drives aberrant endothelial activation. Dr Gordon’s research aims to unravel the mechanisms underpinning the endothelial dysfunction in both acute and long COVID-19. By understanding the inflammatory response and how this reprograms ECs to promote coagulation and endotheliopathy, they will identify the anti-inflammatory therapies that are likely to suppress vascular complications of SARS-CoV-2 infection.
Researcher biography