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10.1159/000524560 http://scihub22266oqcxt.onion/10.1159/000524560 35545011!9801253!35545011     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 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\35545011.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Innate+Immun 2022 ; 14 (6): 643-656 Nephropedia Template TP {{tp|p=35545011|t=2022. IL-1 Mediates Tissue-Specific Inflammation and Severe Respiratory Failure in COVID-19 |pdf=|usr=}}{{35545011}} gab.com Text IL-1 Mediates Tissue-Specific Inflammation and Severe Respiratory Failure in COVID-19 JO: J Innate Immun http://www.kidney.de/pget.php?&tw=1&pmid=35545011 #FOAvip Acute respiratory distress syndrome (ARDS) in COVID-19 has been associated with catastrophic inflammation. We present measurements in humans and a new animal model implicating a role in danger-associated molecular patterns. Calprotectin (S100A8/A9) and high-mobility group box 1 (HMGB1) were measured in patients without/with ARDS, and admission calprotectin was associated with soluble urokinase plasminogen activator receptor (suPAR). An animal model was developed by intravenous injection of plasma from healthy or patients with COVID-19 ARDS into C57/BL6 mice once daily for 3 consecutive days. Mice were treated with one anti-S100A8/A9 antibody, the IL-1 receptor antagonist anakinra or vehicle, and Flo1-2a anti-murine anti-IL-1alpha monoclonal antibody or the specific antihuman IL-1alpha antibody XB2001 or isotype controls. Cytokines and myeloperoxidase (MPO) were measured in tissues. Calprotectin, but not HMGB1, was elevated in ARDS. Higher suPAR indicated higher calprotectin. Animal challenge with COVID-19 plasma led to inflammatory reactions in murine lung and intestines as evidenced by increased levels of TNFalpha, IL-6, IFNgamma, and MPO. Lung inflammation was attenuated with anti-S100A8/A9 pre-treatment. Anakinra treatment restored these levels. Similar decrease was found in mice treated with Flo1-2a but not with XB2001. Circulating alarmins, specifically calprotectin, of critically ill COVID-19 patients induces tissue-specific inflammatory responses through an IL-1-mediated mechanism. This could be attenuated through inhibition of IL-1 receptor or of IL-1alpha. Twit Text FOAVip IL-1 Mediates Tissue-Specific Inflammation and Severe Respiratory Failure in COVID-19 ????J Innate Immun http://www.kidney.de/pget.php?&tw=1&pmid=35545011 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35545011 #FOAvip English Wikipedia <ref>{{Cite pmid|35545011}}</ref> IL-1 Mediates Tissue-Specific Inflammation and Severe Respiratory Failure in COVID-19 #MMPMID35545011 Renieris G; Karakike E; Gkavogianni T; Droggiti DE; Stylianakis E; Andriopoulou T; Spanou VM; Kafousopoulos D; Netea MG; Eugen-Olsen J; Simard J; Giamarellos-Bourboulis EJ J Innate Immun 2022[]; 14 (6): 643-656 PMID35545011show ga Acute respiratory distress syndrome (ARDS) in COVID-19 has been associated with catastrophic inflammation. We present measurements in humans and a new animal model implicating a role in danger-associated molecular patterns. Calprotectin (S100A8/A9) and high-mobility group box 1 (HMGB1) were measured in patients without/with ARDS, and admission calprotectin was associated with soluble urokinase plasminogen activator receptor (suPAR). An animal model was developed by intravenous injection of plasma from healthy or patients with COVID-19 ARDS into C57/BL6 mice once daily for 3 consecutive days. Mice were treated with one anti-S100A8/A9 antibody, the IL-1 receptor antagonist anakinra or vehicle, and Flo1-2a anti-murine anti-IL-1alpha monoclonal antibody or the specific antihuman IL-1alpha antibody XB2001 or isotype controls. Cytokines and myeloperoxidase (MPO) were measured in tissues. Calprotectin, but not HMGB1, was elevated in ARDS. Higher suPAR indicated higher calprotectin. Animal challenge with COVID-19 plasma led to inflammatory reactions in murine lung and intestines as evidenced by increased levels of TNFalpha, IL-6, IFNgamma, and MPO. Lung inflammation was attenuated with anti-S100A8/A9 pre-treatment. Anakinra treatment restored these levels. Similar decrease was found in mice treated with Flo1-2a but not with XB2001. Circulating alarmins, specifically calprotectin, of critically ill COVID-19 patients induces tissue-specific inflammatory responses through an IL-1-mediated mechanism. This could be attenuated through inhibition of IL-1 receptor or of IL-1alpha. |*COVID-19[MESH] |*Respiratory Insufficiency[MESH] |Animals[MESH] |Humans[MESH] |Mice[MESH]IL-1 Mediates Tissue-Specific Inflammation and Severe Respiratory Fail(epmc).pdf DeepDyve Pubget Overpricing