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10.1016/j.lfs.2020.118166 http://scihub22266oqcxt.onion/10.1016/j.lfs.2020.118166 32739471!7392886!32739471     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Life+Sci 2020 ; 258 (ä): 118166 Nephropedia Template TP {{tp|p=32739471|t=2020. The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach |pdf=|usr=}}{{32739471}} gab.com Text The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach JO: Life Sci http://www.kidney.de/pget.php?&tw=1&pmid=32739471 #FOAvip In this paper, a model is proposed of the pathophysiological processes of COVID-19 starting from the infection of human type II alveolar epithelial cells (pneumocytes) by SARS-CoV-2 and culminating in the development of ARDS. The innate immune response to infection of type II alveolar epithelial cells leads both to their death by apoptosis and pyroptosis and to alveolar macrophage activation. Activated macrophages secrete proinflammatory cytokines and chemokines and tend to polarise into the inflammatory M1 phenotype. These changes are associated with activation of vascular endothelial cells and thence the recruitment of highly toxic neutrophils and inflammatory activated platelets into the alveolar space. Activated vascular endothelial cells become a source of proinflammatory cytokines and reactive oxygen species (ROS) and contribute to the development of coagulopathy, systemic sepsis, a cytokine storm and ARDS. Pulmonary activated platelets are also an important source of proinflammatory cytokines and ROS, as well as exacerbating pulmonary neutrophil-mediated inflammatory responses and contributing to systemic sepsis by binding to neutrophils to form platelet-neutrophil complexes (PNCs). PNC formation increases neutrophil recruitment, activation priming and extraversion of these immune cells into inflamed pulmonary tissue, thereby contributing to ARDS. Sequestered PNCs cause the development of a procoagulant and proinflammatory environment. The contribution to ARDS of increased extracellular histone levels, circulating mitochondrial DNA, the chromatin protein HMGB1, decreased neutrophil apoptosis, impaired macrophage efferocytosis, the cytokine storm, the toll-like receptor radical cycle, pyroptosis, necroinflammation, lymphopenia and a high Th17 to regulatory T lymphocyte ratio are detailed. Twit Text FOAVip The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach ????Life Sci http://www.kidney.de/pget.php?&tw=1&pmid=32739471 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32739471 #FOAvip English Wikipedia <ref>{{Cite pmid|32739471}}</ref> The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach #MMPMID32739471 Morris G; Bortolasci CC; Puri BK; Olive L; Marx W; O'Neil A; Athan E; Carvalho AF; Maes M; Walder K; Berk M Life Sci 2020[Oct]; 258 (ä): 118166 PMID32739471show ga In this paper, a model is proposed of the pathophysiological processes of COVID-19 starting from the infection of human type II alveolar epithelial cells (pneumocytes) by SARS-CoV-2 and culminating in the development of ARDS. The innate immune response to infection of type II alveolar epithelial cells leads both to their death by apoptosis and pyroptosis and to alveolar macrophage activation. Activated macrophages secrete proinflammatory cytokines and chemokines and tend to polarise into the inflammatory M1 phenotype. These changes are associated with activation of vascular endothelial cells and thence the recruitment of highly toxic neutrophils and inflammatory activated platelets into the alveolar space. Activated vascular endothelial cells become a source of proinflammatory cytokines and reactive oxygen species (ROS) and contribute to the development of coagulopathy, systemic sepsis, a cytokine storm and ARDS. Pulmonary activated platelets are also an important source of proinflammatory cytokines and ROS, as well as exacerbating pulmonary neutrophil-mediated inflammatory responses and contributing to systemic sepsis by binding to neutrophils to form platelet-neutrophil complexes (PNCs). PNC formation increases neutrophil recruitment, activation priming and extraversion of these immune cells into inflamed pulmonary tissue, thereby contributing to ARDS. Sequestered PNCs cause the development of a procoagulant and proinflammatory environment. The contribution to ARDS of increased extracellular histone levels, circulating mitochondrial DNA, the chromatin protein HMGB1, decreased neutrophil apoptosis, impaired macrophage efferocytosis, the cytokine storm, the toll-like receptor radical cycle, pyroptosis, necroinflammation, lymphopenia and a high Th17 to regulatory T lymphocyte ratio are detailed. |Alveolar Epithelial Cells/immunology/pathology[MESH] |Animals[MESH] |Betacoronavirus/immunology/*physiology[MESH] |COVID-19[MESH] |Coronavirus Infections/complications/immunology/*physiopathology/therapy[MESH] |Humans[MESH] |Immunity, Innate[MESH] |Inflammation/etiology/immunology/physiopathology/therapy[MESH] |Macrophage Activation[MESH] |Macrophages, Alveolar/immunology/pathology[MESH] |Neutrophil Activation[MESH] |Pandemics[MESH] |Platelet Activation[MESH] |Pneumonia, Viral/complications/immunology/*physiopathology/therapy[MESH] |Respiratory Distress Syndrome/etiology/immunology/*physiopathology/therapy[MESH] |SARS-CoV-2[MESH]The pathophysiology of SARS-CoV-2: A suggested model and therapeutic a(epmc).pdf DeepDyve Pubget Overpricing