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10.1164/rccm.202005-1583OC http://scihub22266oqcxt.onion/10.1164/rccm.202005-1583OC 32584597!7491404!32584597     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Respir+Crit+Care+Med 2020 ; 202 (6): 812-821 Nephropedia Template TP {{tp|p=32584597|t=2020. Characterization of the Inflammatory Response to Severe COVID-19 Illness |pdf=|usr=}}{{32584597}} gab.com Text Characterization of the Inflammatory Response to Severe COVID-19 Illness JO: Am J Respir Crit Care Med http://www.kidney.de/pget.php?&tw=1&pmid=32584597 #FOAvip Rationale: Coronavirus disease (COVID-19) is a global threat to health. Its inflammatory characteristics are incompletely understood.Objectives: To define the cytokine profile of COVID-19 and to identify evidence of immunometabolic alterations in those with severe illness.Methods: Levels of IL-1beta, IL-6, IL-8, IL-10, and sTNFR1 (soluble tumor necrosis factor receptor 1) were assessed in plasma from healthy volunteers, hospitalized but stable patients with COVID-19 (COVID(stable) patients), patients with COVID-19 requiring ICU admission (COVID(ICU) patients), and patients with severe community-acquired pneumonia requiring ICU support (CAP(ICU) patients). Immunometabolic markers were measured in circulating neutrophils from patients with severe COVID-19. The acute phase response of AAT (alpha-1 antitrypsin) to COVID-19 was also evaluated.Measurements and Main Results: IL-1beta, IL-6, IL-8, and sTNFR1 were all increased in patients with COVID-19. COVID(ICU) patients could be clearly differentiated from COVID(stable) patients, and demonstrated higher levels of IL-1beta, IL-6, and sTNFR1 but lower IL-10 than CAP(ICU) patients. COVID-19 neutrophils displayed altered immunometabolism, with increased cytosolic PKM2 (pyruvate kinase M2), phosphorylated PKM2, HIF-1alpha (hypoxia-inducible factor-1alpha), and lactate. The production and sialylation of AAT increased in COVID-19, but this antiinflammatory response was overwhelmed in severe illness, with the IL-6:AAT ratio markedly higher in patients requiring ICU admission (P < 0.0001). In critically unwell patients with COVID-19, increases in IL-6:AAT predicted prolonged ICU stay and mortality, whereas improvement in IL-6:AAT was associated with clinical resolution (P < 0.0001).Conclusions: The COVID-19 cytokinemia is distinct from that of other types of pneumonia, leading to organ failure and ICU need. Neutrophils undergo immunometabolic reprogramming in severe COVID-19 illness. Cytokine ratios may predict outcomes in this population. Twit Text FOAVip Characterization of the Inflammatory Response to Severe COVID-19 Illness ????Am J Respir Crit Care Med http://www.kidney.de/pget.php?&tw=1&pmid=32584597 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32584597 #FOAvip English Wikipedia <ref>{{Cite pmid|32584597}}</ref> Characterization of the Inflammatory Response to Severe COVID-19 Illness #MMPMID32584597 McElvaney OJ; McEvoy NL; McElvaney OF; Carroll TP; Murphy MP; Dunlea DM; Ni Choileain O; Clarke J; O'Connor E; Hogan G; Ryan D; Sulaiman I; Gunaratnam C; Branagan P; O'Brien ME; Morgan RK; Costello RW; Hurley K; Walsh S; de Barra E; McNally C; McConkey S; Boland F; Galvin S; Kiernan F; O'Rourke J; Dwyer R; Power M; Geoghegan P; Larkin C; O'Leary RA; Freeman J; Gaffney A; Marsh B; Curley GF; McElvaney NG Am J Respir Crit Care Med 2020[Sep]; 202 (6): 812-821 PMID32584597show ga Rationale: Coronavirus disease (COVID-19) is a global threat to health. Its inflammatory characteristics are incompletely understood.Objectives: To define the cytokine profile of COVID-19 and to identify evidence of immunometabolic alterations in those with severe illness.Methods: Levels of IL-1beta, IL-6, IL-8, IL-10, and sTNFR1 (soluble tumor necrosis factor receptor 1) were assessed in plasma from healthy volunteers, hospitalized but stable patients with COVID-19 (COVID(stable) patients), patients with COVID-19 requiring ICU admission (COVID(ICU) patients), and patients with severe community-acquired pneumonia requiring ICU support (CAP(ICU) patients). Immunometabolic markers were measured in circulating neutrophils from patients with severe COVID-19. The acute phase response of AAT (alpha-1 antitrypsin) to COVID-19 was also evaluated.Measurements and Main Results: IL-1beta, IL-6, IL-8, and sTNFR1 were all increased in patients with COVID-19. COVID(ICU) patients could be clearly differentiated from COVID(stable) patients, and demonstrated higher levels of IL-1beta, IL-6, and sTNFR1 but lower IL-10 than CAP(ICU) patients. COVID-19 neutrophils displayed altered immunometabolism, with increased cytosolic PKM2 (pyruvate kinase M2), phosphorylated PKM2, HIF-1alpha (hypoxia-inducible factor-1alpha), and lactate. The production and sialylation of AAT increased in COVID-19, but this antiinflammatory response was overwhelmed in severe illness, with the IL-6:AAT ratio markedly higher in patients requiring ICU admission (P < 0.0001). In critically unwell patients with COVID-19, increases in IL-6:AAT predicted prolonged ICU stay and mortality, whereas improvement in IL-6:AAT was associated with clinical resolution (P < 0.0001).Conclusions: The COVID-19 cytokinemia is distinct from that of other types of pneumonia, leading to organ failure and ICU need. Neutrophils undergo immunometabolic reprogramming in severe COVID-19 illness. Cytokine ratios may predict outcomes in this population. |Acute-Phase Reaction/*immunology/metabolism[MESH] |Adult[MESH] |Aged[MESH] |Betacoronavirus[MESH] |Blotting, Western[MESH] |COVID-19[MESH] |Carrier Proteins/*metabolism[MESH] |Case-Control Studies[MESH] |Community-Acquired Infections/immunology/metabolism[MESH] |Coronavirus Infections/*immunology/*metabolism/mortality/physiopathology[MESH] |Critical Illness[MESH] |Cytokines/*immunology[MESH] |Electrophoresis, Polyacrylamide Gel[MESH] |Enzyme-Linked Immunosorbent Assay[MESH] |Female[MESH] |Hospitalization[MESH] |Humans[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism[MESH] |Intensive Care Units[MESH] |Interleukin-10/immunology[MESH] |Interleukin-1beta/immunology[MESH] |Interleukin-6/immunology[MESH] |Interleukin-8/immunology[MESH] |Lactic Acid/*metabolism[MESH] |Length of Stay[MESH] |Male[MESH] |Membrane Proteins/*metabolism[MESH] |Middle Aged[MESH] |Neutrophils/immunology/metabolism[MESH] |Pandemics[MESH] |Phosphorylation[MESH] |Pneumonia, Viral/*immunology/*metabolism/mortality/physiopathology[MESH] |Pneumonia/immunology/metabolism[MESH] |Receptors, Tumor Necrosis Factor, Type I/immunology[MESH] |SARS-CoV-2[MESH] |Severity of Illness Index[MESH] |Thyroid Hormone-Binding Proteins[MESH] |Thyroid Hormones/*metabolism[MESH]Characterization of the Inflammatory Response to Severe COVID-19 Illne(epmc).pdf DeepDyve Pubget Overpricing