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10.3389/fimmu.2020.621441 http://scihub22266oqcxt.onion/10.3389/fimmu.2020.621441 33584719!7876321!33584719     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 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\33584719.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Immunol 2020 ; 11 (ä): 621441 Nephropedia Template TP {{tp|p=33584719|t=2020. Cytokine Signature Induced by SARS-CoV-2 Spike Protein in a Mouse Model |pdf=|usr=}}{{33584719}} gab.com Text Cytokine Signature Induced by SARS-CoV-2 Spike Protein in a Mouse Model JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33584719 #FOAvip Although COVID-19 has become a major challenge to global health, there are currently no efficacious agents for effective treatment. Cytokine storm syndrome (CSS) can lead to acute respiratory distress syndrome (ARDS), which contributes to most COVID-19 mortalities. Research points to interleukin 6 (IL-6) as a crucial signature of the cytokine storm, and the clinical use of the IL-6 inhibitor tocilizumab shows potential for treatment of COVID-19 patient. In this study, we challenged wild-type and adenovirus-5/human angiotensin-converting enzyme 2-expressing BALB/c mice with a combination of polyinosinic-polycytidylic acid and recombinant SARS-CoV-2 spike-extracellular domain protein. High levels of TNF-alpha and nearly 100 times increased IL-6 were detected at 6 h, but disappeared by 24 h in bronchoalveolar lavage fluid (BALF) following immunostimulant challenge. Lung injury observed by histopathologic changes and magnetic resonance imaging at 24 h indicated that increased TNF-alpha and IL-6 may initiate CSS in the lung, resulting in the continual production of inflammatory cytokines. We hypothesize that TNF-alpha and IL-6 may contribute to the occurrence of CSS in COVID-19. We also investigated multiple monoclonal antibodies (mAbs) and inhibitors for neutralizing the pro-inflammatory phenotype of COVID-19: mAbs against IL-1alpha, IL-6, TNF-alpha, and granulocyte-macrophage colony-stimulating factor (GM-CSF), and inhibitors of p38 and JAK partially relieved CSS; mAbs against IL-6, TNF-alpha, and GM-CSF, and inhibitors of p38, extracellular signal-regulated kinase, and myeloperoxidase somewhat reduced neutrophilic alveolitis in the lung. This novel murine model opens a biologically safe, time-saving avenue for clarifying the mechanism of CSS/ARDS in COVID-19 and developing new therapeutic drugs. Twit Text FOAVip Cytokine Signature Induced by SARS-CoV-2 Spike Protein in a Mouse Model ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=33584719 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33584719 #FOAvip English Wikipedia <ref>{{Cite pmid|33584719}}</ref> Cytokine Signature Induced by SARS-CoV-2 Spike Protein in a Mouse Model #MMPMID33584719 Gu T; Zhao S; Jin G; Song M; Zhi Y; Zhao R; Ma F; Zheng Y; Wang K; Liu H; Xin M; Han W; Li X; Dong CD; Liu K; Dong Z Front Immunol 2020[]; 11 (ä): 621441 PMID33584719show ga Although COVID-19 has become a major challenge to global health, there are currently no efficacious agents for effective treatment. Cytokine storm syndrome (CSS) can lead to acute respiratory distress syndrome (ARDS), which contributes to most COVID-19 mortalities. Research points to interleukin 6 (IL-6) as a crucial signature of the cytokine storm, and the clinical use of the IL-6 inhibitor tocilizumab shows potential for treatment of COVID-19 patient. In this study, we challenged wild-type and adenovirus-5/human angiotensin-converting enzyme 2-expressing BALB/c mice with a combination of polyinosinic-polycytidylic acid and recombinant SARS-CoV-2 spike-extracellular domain protein. High levels of TNF-alpha and nearly 100 times increased IL-6 were detected at 6 h, but disappeared by 24 h in bronchoalveolar lavage fluid (BALF) following immunostimulant challenge. Lung injury observed by histopathologic changes and magnetic resonance imaging at 24 h indicated that increased TNF-alpha and IL-6 may initiate CSS in the lung, resulting in the continual production of inflammatory cytokines. We hypothesize that TNF-alpha and IL-6 may contribute to the occurrence of CSS in COVID-19. We also investigated multiple monoclonal antibodies (mAbs) and inhibitors for neutralizing the pro-inflammatory phenotype of COVID-19: mAbs against IL-1alpha, IL-6, TNF-alpha, and granulocyte-macrophage colony-stimulating factor (GM-CSF), and inhibitors of p38 and JAK partially relieved CSS; mAbs against IL-6, TNF-alpha, and GM-CSF, and inhibitors of p38, extracellular signal-regulated kinase, and myeloperoxidase somewhat reduced neutrophilic alveolitis in the lung. This novel murine model opens a biologically safe, time-saving avenue for clarifying the mechanism of CSS/ARDS in COVID-19 and developing new therapeutic drugs. |*Disease Models, Animal[MESH] |Animals[MESH] |Anti-Inflammatory Agents/*pharmacology[MESH] |Antibodies, Neutralizing/pharmacology[MESH] |Antibodies, Viral/pharmacology[MESH] |COVID-19/*immunology[MESH] |Cytokine Release Syndrome/*immunology/virology[MESH] |Cytokines/immunology[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred BALB C[MESH] |Poly I-C/immunology[MESH] |SARS-CoV-2/immunology[MESH]Cytokine Signature Induced by SARS-CoV-2 Spike Protein in a Mouse Mode(epmc).pdf DeepDyve Pubget Overpricing