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10.1002/eji.202049159 http://scihub22266oqcxt.onion/10.1002/eji.202049159 34107055!8237023!34107055     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Eur+J+Immunol 2021 ; 51 (9): 2330-2340 Nephropedia Template TP {{tp|p=34107055|t=2021. Tofacitinib therapy intercepts macrophage metabolic reprogramming instigated by SARS-CoV-2 Spike protein |pdf=|usr=}}{{34107055}} gab.com Text Tofacitinib therapy intercepts macrophage metabolic reprogramming instigated by SARS-CoV-2 Spike protein JO: Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34107055 #FOAvip The molecular mechanism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Spike protein was characterized to identify novel therapies. The impact of tofacitinib, IL-6R Ab, or TNFi therapy was determined on Spike protein or LPS/IFN-gamma-induced signaling, inflammation, and metabolic reprogramming in MPhis and/or rheumatoid arthritis (RA) fibroblast-like synoviocyte (FLS). ACE2 frequency was markedly expanded in MPhis compared to T cells and RA FLS. Tofacitinib suppresses Spike protein potentiated STAT1 signaling, whereas this function was unchanged by TNFi. Tofacitinib impairs IL-6/IFN/LPS-induced STAT1 and STAT3 phosphorylation in RA MPhis and FLS. Interestingly, tofacitinib had a broader inhibitory effect on the monokines, glycolytic regulators, or oxidative metabolites compared to IL-6R Ab and TNFi in Spike-protein-activated MPhis. In contrast, all three therapies disrupted IFN-alpha and IFN-beta secretion in response to Spike protein; nonetheless, the IFN-gamma was only curtailed by tofacitinib or IL-6R Ab. While tofacitinib counteracted MPhi metabolic rewiring instigated by Spike protein, it was inconsequential on the glycolysis expansion mediated via HK2 and/or LDHA in the activated RA MPhi and FLS. Nevertheless, the potentiated inflammatory response and the diminished oxidative phosphorylation modulated by Spike protein and/or LPS/IFN-gamma stimulation in MPhis or RA FLS were reversed by tofacitinib. In conclusion, tofacitinib suppresses MPhi inflammation and immunometabolism triggered by Spike protein and may provide a promising strategy for COVID-19 patients. Twit Text FOAVip Tofacitinib therapy intercepts macrophage metabolic reprogramming instigated by SARS-CoV-2 Spike protein ????Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34107055 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34107055 #FOAvip English Wikipedia <ref>{{Cite pmid|34107055}}</ref> Tofacitinib therapy intercepts macrophage metabolic reprogramming instigated by SARS-CoV-2 Spike protein #MMPMID34107055 Palasiewicz K; Umar S; Romay B; Zomorrodi RK; Shahrara S Eur J Immunol 2021[Sep]; 51 (9): 2330-2340 PMID34107055show ga The molecular mechanism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Spike protein was characterized to identify novel therapies. The impact of tofacitinib, IL-6R Ab, or TNFi therapy was determined on Spike protein or LPS/IFN-gamma-induced signaling, inflammation, and metabolic reprogramming in MPhis and/or rheumatoid arthritis (RA) fibroblast-like synoviocyte (FLS). ACE2 frequency was markedly expanded in MPhis compared to T cells and RA FLS. Tofacitinib suppresses Spike protein potentiated STAT1 signaling, whereas this function was unchanged by TNFi. Tofacitinib impairs IL-6/IFN/LPS-induced STAT1 and STAT3 phosphorylation in RA MPhis and FLS. Interestingly, tofacitinib had a broader inhibitory effect on the monokines, glycolytic regulators, or oxidative metabolites compared to IL-6R Ab and TNFi in Spike-protein-activated MPhis. In contrast, all three therapies disrupted IFN-alpha and IFN-beta secretion in response to Spike protein; nonetheless, the IFN-gamma was only curtailed by tofacitinib or IL-6R Ab. While tofacitinib counteracted MPhi metabolic rewiring instigated by Spike protein, it was inconsequential on the glycolysis expansion mediated via HK2 and/or LDHA in the activated RA MPhi and FLS. Nevertheless, the potentiated inflammatory response and the diminished oxidative phosphorylation modulated by Spike protein and/or LPS/IFN-gamma stimulation in MPhis or RA FLS were reversed by tofacitinib. In conclusion, tofacitinib suppresses MPhi inflammation and immunometabolism triggered by Spike protein and may provide a promising strategy for COVID-19 patients. |*COVID-19 Drug Treatment[MESH] |Arthritis, Rheumatoid/metabolism[MESH] |COVID-19/metabolism[MESH] |Cells, Cultured[MESH] |Fibroblasts/drug effects/metabolism[MESH] |Humans[MESH] |Interleukin-6/metabolism[MESH] |Macrophages/*drug effects/metabolism[MESH] |Piperidines/*pharmacology[MESH] |Pyrimidines/*pharmacology[MESH] |Receptors, Interleukin-6/metabolism[MESH] |SARS-CoV-2/*drug effects[MESH] |STAT1 Transcription Factor/metabolism[MESH] |STAT3 Transcription Factor/metabolism[MESH] |Signal Transduction/drug effects[MESH] |Spike Glycoprotein, Coronavirus/*metabolism[MESH]Tofacitinib therapy intercepts macrophage metabolic reprogramming inst(epmc).pdf DeepDyve Pubget Overpricing