Ntributions: J.L.C. planned the project, developed and performed the experiments, analysed the data and wrote the manuscript; S.B. performed ischaemia eperfusion surgery. S.H. performed and analysed the chemotaxis assays. S.M. performed the immunofluorescence experiments. V.B. performed the Ca2 flux experiments. M.P. contributed towards the project arranging and writing in the manuscript. CONFLICT OF INTEREST The authors declare that they’ve no conflict of interest.1 0 0 6 EMBO reports VOL 14 NO 11 Chemerin peptides modulate neutrophil reactivity J.L. Money et al
Arteriosclerosis, Thrombosis, and Vascular Biology CLINICAL AND POPULATION STUDIESPlatelets Promote Thromboinflammation in SARS-CoV-2 PneumoniaFrancesco Taus, Gianluca Salvagno, Stefania Can Cristiano Fava , Fulvia Mazzaferri, Elena Carrara, Varvara Petrova , Roza Maria Barouni, Francesco Dima, Andrea Dalbeni, Simone Romano, Giovanni Poli, Marco Benati , Simone De Nitto , Giancarlo Mansueto , Manuela Iezzi , Evelina Tacconelli, Giuseppe Lippi , Vincenzo Bronte , Pietro MinuzOBJECTIVE: Pulmonary thrombosis is observed in severe acute respiratory syndrome coronavirus 2 pneumonia. Aim was to investigate whether subpopulations of platelets had been programmed to procoagulant and inflammatory activities in coronavirus disease 2019 (COVID-19) individuals with pneumonia, with no comorbidities predisposing to thromboembolism. Strategy AND CXCL17 Proteins Recombinant Proteins Results: General, 37 individuals and 28 healthful subjects were studied. Platelet-leukocyte aggregates, plateletderived microvesicles, the expression of P-selectin, and active fibrinogen receptor on platelets have been quantified by flow cytometry. The profile of 45 cytokines, chemokines, and development variables released by platelets was defined by immunoassay. The contribution of platelets to coagulation factor activity was selectively measured. Many platelet-monocyte (imply E, 67.9.9 , n=17 versus 19.four.0 , n=22; P0.0001) and platelet-granulocyte conjugates (34.two.04 versus 8.6.7 ; P0.0001) were detected in patients. Resting patient platelets had similar levels of P-selectin (ten.9.6 , n=12) to collagenactivated control platelets (eight.7.5), which was not further elevated by collagen activation on patient platelets (12.4.5 , P=nonsignificant). The agonist-stimulated expression of the active fibrinogen receptor was decreased by 60 in patients (P0.0001 versus controls). Cytokines (IL [interleukin]-1, IL-1, IL-1RA, IL-4, IL-10, IL-13, IL, 17, IL-27, IFN [interferon], and IFN-), chemokines (MCP-1/CCL2 [monocyte chemoattractant protein 1]), and development variables (VEGF [vascular endothelial growth factor]-A/D) were released in considerably larger amounts upon stimulation of COVID-19 platelets. Platelets contributed to increased fibrinogen, VWF (von Willebrand aspect), and element XII in COVID-19 patients. Patients (28.five.7 s, n=32), as opposed to controls (31.6.five s, n=28; P0.001), showed accelerated issue XII ependent coagulation. CONCLUSIONS: Platelets in COVID-19 pneumonia are primed to spread proinflammatory and procoagulant activities in systemic circulation. GRAPHIC ABSTRACT: A graphic CXCL9 Proteins Accession abstract is obtainable for this short article.Important Words: blood platelets inflammation interferons monocytes thrombosisThe coronavirus illness 2019 (COVID-19) pandemic, caused by the serious acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is associated with high mortality rate, attributed towards the severity of pneumonia along with the development of systemic complications, which includes target-organ harm and thromboem.
