apyrase and Influenza--Human

CD39/NTPDase1 has emerged as an important molecule that contributes to maintain inflammatory and coagulatory homeostasis. Various studies have hypothesized the possible role of CD39 in COVID-19 pathophysiology since no confirmatory data shed light in this regard. Therefore, we aimed to quantify CD39 expression on COVID-19 patients exploring its association with severity clinical parameters and ICU admission, while unraveling the role of purinergic signaling on thromboinflammation in COVID-19 patients. We selected a prospective cohort of patients hospitalized due to severe COVID-19 pneumonia (n=75), a historical cohort of Influenza A pneumonia patients (n=18) and sex/age-matched healthy controls (n=30). CD39 was overexpressed in COVID-19 patients' plasma and immune cell subsets and related to hypoxemia. Plasma soluble form of CD39 (sCD39) was related to length of hospital stay and independently associated with intensive care unit admission (adjusted odds ratio 1.04, 95%CI 1.0-1.08, p=0.038), with a net reclassification index of 0.229 (0.118-0.287; p=0.036). COVID-19 patients showed extracellular accumulation of adenosine nucleotides (ATP and ADP), resulting in systemic inflammation and pro-coagulant state, as a consequence of purinergic pathway dysregulation. Interestingly, we found that COVID-19 plasma caused platelet activation, which was successfully blocked by the P2Y

Topics: Adenosine Diphosphate; Adenosine Triphosphate; Apyrase; Biomarkers; Blood Platelets; Cell Hypoxia; COVID-19; Critical Care; Female; Humans; Influenza A virus; Influenza, Human; Length of Stay; Male; Middle Aged; Platelet Activation; Prognosis; Prospective Studies; Purinergic P2Y Receptor Antagonists; Receptors, Purinergic P2Y; SARS-CoV-2; Severity of Illness Index; Signal Transduction; Thromboinflammation; Ticagrelor