For a study, it was determined that COVID-19 had prompted researchers to better understand its pathogenesis in order to develop novel treatment methods. While risk factors such as older age, obesity, and diabetes mellitus suggested that endothelial cells (ECs) played an important role, autopsies revealed clots in the pulmonary microvasculature that were rich in neutrophils, and DNA traps produced by these cells were known as neutrophil extracellular traps (NETs.) Microparticles (MPs) were submicron extracellular vesicles that were implicated in pro-inflammatory pathways in a variety of disorders. As a result, researchers examined 3 patient groups: one without intubation, one with intubation, and one after extubation. 

When compared to uninfected controls, platelet-derived MPs and endothelial cell (EC)-derived MPs were more concentrated and larger in the most severe group, the intubated group. MPs from patients with COVID-19 who were intubated caused EC mortality and increased the expression of two adhesion molecules: P-selectin and vascular cell adhesion molecule-1 (VCAM-1). Surprisingly, upon incubation with these ECs, neutrophil adhesion and NET production increased. They also discovered that pre incubating these COVID-19 MPs with the phosphatidylserine capping endogenous protein, annexin A5, reduced cytotoxicity, P-selectin, and VCAM-1 induction, as well as increases in neutrophil adherence and NET release. The findings showed that MPs play an important role in COVID-19 pathogenesis and led to annexin A5 as a possible therapy.