Platelets-monocytes aggregates in COVID19 pathogenesis

Abstract

There is an urgent need to understand the pathogenesis of coronavirus disease 2019 (COVID19). In particular, thrombotic complications in patients with COVID19 are common and contribute to organ failure and mortality. It has been reported that COVID19 patients present increased platelet activation. Our aim was to evaluate if activated platelets from COVID19 patients form aggregates with monocytes and modulate their activation and functionality. Samples from whole blood and PBMCs were obtained from healthy donors or COViD19 patients. PBMCs were purified by ficoll-paque and washed platelets were obtained from plasma by centrifugation with 200 nM of prostaglandin I2 . Phenotype and cytokine production was evaluated by flow cytometry and ELISA. The viral production was measured by cytopathic effect in Vero cells. We observed that COVID19 patients presented an increased percentage of platelet-monocyte aggregates compared to control samples (7,1 ± 1,9, n=10; 44,3 ± 3,9, n=30, p<0,0001). We did not observe a correlation between platelet-monocyte aggregates and severity of the disease. When we analyzed the functionality of monocytes we found that COVID19 patients presented an increased production of IL8 (n=4, p<0,05) in monocytes aggregated with platelets but not of TNFα and IL6 (n=6). We also evaluated the role of platelets in the dissemination of the virus. Interestingly, we observed that COVID19 platelets but not control platelets, inhibited the infection of SARS-CoV-2 in Vero cells (n=2, p<0,05). These results show that patients COVID19 present increased platelet-monocyte aggregates. Further studies are required to evaluate the role of these aggregates and platelets in SARS-CoV-2 pathogenesis.