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10.1182/bloodadvances.2021006680 http://scihub22266oqcxt.onion/10.1182/bloodadvances.2021006680 35420680!9015715!35420680     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Blood+Adv 2022 ; 6 (17): 5085-5099 Nephropedia Template TP {{tp|p=35420680|t=2022. Platelet-monocyte interaction amplifies thromboinflammation through tissue factor signaling in COVID-19 |pdf=|usr=}}{{35420680}} gab.com Text Platelet-monocyte interaction amplifies thromboinflammation through tissue factor signaling in COVID-19 JO: Blood Adv http://www.kidney.de/pget.php?&tw=1&pmid=35420680 #FOAvip Accumulating evidence into the pathogenesis of COVID-19 highlights a hypercoagulability state with high risk of life-threatening thromboembolic complications. However, the mechanisms of hypercoagulability and their link to hyperinflammation remain poorly understood. Here, we investigate functions and mechanisms of platelet activation and platelet-monocyte interactions in inflammatory amplification during SARS-CoV-2 infection. We used a combination of immunophenotyping, single-cell analysis, functional assays, and pharmacological approaches to gain insights on mechanisms. Critically ill patients with COVID-19 exhibited increased platelet-monocyte aggregates formation. We identified a subset of inflammatory monocytes presenting high CD16 and low HLA-DR expression as the subset mainly interacting with platelets during severe COVID-19. Single-cell RNA-sequencing analysis indicated enhanced fibrinogen receptor Mac-1 in monocytes from patients with severe COVID-19. Monocytes from patients with severe COVID-19 displayed increased platelet binding and hyperresponsiveness to P-selectin and fibrinogen with respect to tumor necrosis factor-alpha and interleukin-1beta secretion. Platelets were able to orchestrate monocyte responses driving tissue factor (TF) expression, inflammatory activation, and inflammatory cytokines secretion in SARS-CoV-2 infection. Platelet-monocyte interactions ex vivo and in SARS-CoV-2 infection model in vitro reciprocally activated monocytes and platelets, inducing the heightened secretion of a wide panel of inflammatory mediators. We identified platelet adhesion as a primary signaling mechanism inducing mediator secretion and TF expression, whereas TF signaling played major roles in amplifying inflammation by inducing proinflammatory cytokines, especially tumor necrosis factor-alpha and interleukin-1beta. Our data identify platelet-induced TF expression and activity at the crossroad of coagulation and inflammation in severe COVID-19. Twit Text FOAVip Platelet-monocyte interaction amplifies thromboinflammation through tissue factor signaling in COVID-19 ????Blood Adv http://www.kidney.de/pget.php?&tw=1&pmid=35420680 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35420680 #FOAvip English Wikipedia <ref>{{Cite pmid|35420680}}</ref> Platelet-monocyte interaction amplifies thromboinflammation through tissue factor signaling in COVID-19 #MMPMID35420680 Hottz ED; Martins-Goncalves R; Palhinha L; Azevedo-Quintanilha IG; de Campos MM; Sacramento CQ; Temerozo JR; Soares VC; Dias SSG; Teixeira L; Castro I; Righy C; Souza TML; Kurtz P; Andrade BB; Nakaya HI; Monteiro RQ; Bozza FA; Bozza PT Blood Adv 2022[Sep]; 6 (17): 5085-5099 PMID35420680show ga Accumulating evidence into the pathogenesis of COVID-19 highlights a hypercoagulability state with high risk of life-threatening thromboembolic complications. However, the mechanisms of hypercoagulability and their link to hyperinflammation remain poorly understood. Here, we investigate functions and mechanisms of platelet activation and platelet-monocyte interactions in inflammatory amplification during SARS-CoV-2 infection. We used a combination of immunophenotyping, single-cell analysis, functional assays, and pharmacological approaches to gain insights on mechanisms. Critically ill patients with COVID-19 exhibited increased platelet-monocyte aggregates formation. We identified a subset of inflammatory monocytes presenting high CD16 and low HLA-DR expression as the subset mainly interacting with platelets during severe COVID-19. Single-cell RNA-sequencing analysis indicated enhanced fibrinogen receptor Mac-1 in monocytes from patients with severe COVID-19. Monocytes from patients with severe COVID-19 displayed increased platelet binding and hyperresponsiveness to P-selectin and fibrinogen with respect to tumor necrosis factor-alpha and interleukin-1beta secretion. Platelets were able to orchestrate monocyte responses driving tissue factor (TF) expression, inflammatory activation, and inflammatory cytokines secretion in SARS-CoV-2 infection. Platelet-monocyte interactions ex vivo and in SARS-CoV-2 infection model in vitro reciprocally activated monocytes and platelets, inducing the heightened secretion of a wide panel of inflammatory mediators. We identified platelet adhesion as a primary signaling mechanism inducing mediator secretion and TF expression, whereas TF signaling played major roles in amplifying inflammation by inducing proinflammatory cytokines, especially tumor necrosis factor-alpha and interleukin-1beta. Our data identify platelet-induced TF expression and activity at the crossroad of coagulation and inflammation in severe COVID-19. |*COVID-19[MESH] |*Thrombophilia[MESH] |*Thrombosis/metabolism[MESH] |Blood Platelets/metabolism[MESH] |Cytokines/metabolism[MESH] |Humans[MESH] |Inflammation/pathology[MESH] |Interleukin-1beta/metabolism[MESH] |Monocytes/metabolism[MESH] |SARS-CoV-2[MESH] |Thromboinflammation[MESH] |Thromboplastin/metabolism[MESH]Platelet-monocyte interaction amplifies thromboinflammation through ti(epmc).pdf DeepDyve Pubget Overpricing