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10.3389/fimmu.2020.01518 http://scihub22266oqcxt.onion/10.3389/fimmu.2020.01518 32655582!7324760!32655582     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Immunol 2020 ; 11 (ä): 1518 Nephropedia Template TP {{tp|p=32655582|t=2020. Targeting the NLRP3 Inflammasome in Severe COVID-19 |pdf=|usr=}}{{32655582}} gab.com Text Targeting the NLRP3 Inflammasome in Severe COVID-19 JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32655582 #FOAvip Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a member of the genus Betacoronavirus within the family Coronaviridae. It is an enveloped single-stranded positive-sense RNA virus. Since December of 2019, a global expansion of the infection has occurred with widespread dissemination of coronavirus disease 2019 (COVID-19). COVID-19 often manifests as only mild cold-like symptomatology, but severe disease with complications occurs in 15% of cases. Respiratory failure occurs in severe disease that can be accompanied by a systemic inflammatory reaction characterized by inflammatory cytokine release. In severe cases, fatality is caused by the rapid development of severe lung injury characteristic of acute respiratory distress syndrome (ARDS). Although ARDS is a complication of SARS-CoV-2 infection, it is not viral replication or infection that causes tissue injury; rather, it is the result of dysregulated hyperinflammation in response to viral infection. This pathology is characterized by intense, rapid stimulation of the innate immune response that triggers activation of the Nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome pathway and release of its products including the proinflammatory cytokines IL-6 and IL-1beta. Here we review the literature that describes the pathogenesis of severe COVID-19 and NLRP3 activation and describe an important role in targeting this pathway for the treatment of severe COVID-19. Twit Text FOAVip Targeting the NLRP3 Inflammasome in Severe COVID-19 ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32655582 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32655582 #FOAvip English Wikipedia <ref>{{Cite pmid|32655582}}</ref> Targeting the NLRP3 Inflammasome in Severe COVID-19 #MMPMID32655582 Freeman TL; Swartz TH Front Immunol 2020[]; 11 (ä): 1518 PMID32655582show ga Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a member of the genus Betacoronavirus within the family Coronaviridae. It is an enveloped single-stranded positive-sense RNA virus. Since December of 2019, a global expansion of the infection has occurred with widespread dissemination of coronavirus disease 2019 (COVID-19). COVID-19 often manifests as only mild cold-like symptomatology, but severe disease with complications occurs in 15% of cases. Respiratory failure occurs in severe disease that can be accompanied by a systemic inflammatory reaction characterized by inflammatory cytokine release. In severe cases, fatality is caused by the rapid development of severe lung injury characteristic of acute respiratory distress syndrome (ARDS). Although ARDS is a complication of SARS-CoV-2 infection, it is not viral replication or infection that causes tissue injury; rather, it is the result of dysregulated hyperinflammation in response to viral infection. This pathology is characterized by intense, rapid stimulation of the innate immune response that triggers activation of the Nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome pathway and release of its products including the proinflammatory cytokines IL-6 and IL-1beta. Here we review the literature that describes the pathogenesis of severe COVID-19 and NLRP3 activation and describe an important role in targeting this pathway for the treatment of severe COVID-19. |Animals[MESH] |Betacoronavirus/*metabolism[MESH] |COVID-19[MESH] |Coronavirus Infections/complications/drug therapy/*metabolism/virology[MESH] |Cytokine Release Syndrome/drug therapy/metabolism[MESH] |Furans[MESH] |Heterocyclic Compounds, 4 or More Rings/pharmacology/therapeutic use[MESH] |Humans[MESH] |Immunity, Innate[MESH] |Indenes[MESH] |Inflammasomes/*antagonists & inhibitors/*metabolism[MESH] |Interleukin 1 Receptor Antagonist Protein/pharmacology/therapeutic use[MESH] |Interleukin-1beta/antagonists & inhibitors/metabolism[MESH] |Mice[MESH] |NLR Family, Pyrin Domain-Containing 3 Protein/*antagonists & inhibitors/*metabolism[MESH] |Pandemics[MESH] |Pneumonia, Viral/complications/drug therapy/*metabolism/virology[MESH] |Pyroptosis/drug effects[MESH] |Respiratory Distress Syndrome/drug therapy/etiology/metabolism[MESH] |SARS-CoV-2[MESH] |Sesquiterpenes, Guaiane/pharmacology/therapeutic use[MESH] |Sulfonamides[MESH]Targeting the NLRP3 Inflammasome in Severe COVID-19 (epmc).pdf DeepDyve Pubget Overpricing