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10.1073/pnas.2116853118 http://scihub22266oqcxt.onion/10.1073/pnas.2116853118 34969849!8740714!34969849     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 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 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Proc+Natl+Acad+Sci+U+S+A 2022 ; 119 (1): ä Nephropedia Template TP {{tp|p=34969849|t=2022. A virus-specific monocyte inflammatory phenotype is induced by SARS-CoV-2 at the immune-epithelial interface |pdf=|usr=}}{{34969849}} gab.com Text A virus-specific monocyte inflammatory phenotype is induced by SARS-CoV-2 at the immune-epithelial interface JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=34969849 #FOAvip Infection by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) provokes a potentially fatal pneumonia with multiorgan failure, and high systemic inflammation. To gain mechanistic insight and ferret out the root of this immune dysregulation, we modeled, by in vitro coculture, the interactions between infected epithelial cells and immunocytes. A strong response was induced in monocytes and B cells, with a SARS-CoV-2-specific inflammatory gene cluster distinct from that seen in influenza A or Ebola virus-infected cocultures, and which reproduced deviations reported in blood or lung myeloid cells from COVID-19 patients. A substantial fraction of the effect could be reproduced after individual transfection of several SARS-CoV-2 proteins (Spike and some nonstructural proteins), mediated by soluble factors, but not via transcriptional induction. This response was greatly muted in monocytes from healthy children, perhaps a clue to the age dependency of COVID-19. These results suggest that the inflammatory malfunction in COVID-19 is rooted in the earliest perturbations that SARS-CoV-2 induces in epithelia. Twit Text FOAVip A virus-specific monocyte inflammatory phenotype is induced by SARS-CoV-2 at the immune-epithelial interface ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=34969849 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34969849 #FOAvip English Wikipedia <ref>{{Cite pmid|34969849}}</ref> A virus-specific monocyte inflammatory phenotype is induced by SARS-CoV-2 at the immune-epithelial interface #MMPMID34969849 Leon J; Michelson DA; Olejnik J; Chowdhary K; Oh HS; Hume AJ; Galvan-Pena S; Zhu Y; Chen F; Vijaykumar B; Yang L; Crestani E; Yonker LM; Knipe DM; Muhlberger E; Benoist C Proc Natl Acad Sci U S A 2022[Jan]; 119 (1): ä PMID34969849show ga Infection by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) provokes a potentially fatal pneumonia with multiorgan failure, and high systemic inflammation. To gain mechanistic insight and ferret out the root of this immune dysregulation, we modeled, by in vitro coculture, the interactions between infected epithelial cells and immunocytes. A strong response was induced in monocytes and B cells, with a SARS-CoV-2-specific inflammatory gene cluster distinct from that seen in influenza A or Ebola virus-infected cocultures, and which reproduced deviations reported in blood or lung myeloid cells from COVID-19 patients. A substantial fraction of the effect could be reproduced after individual transfection of several SARS-CoV-2 proteins (Spike and some nonstructural proteins), mediated by soluble factors, but not via transcriptional induction. This response was greatly muted in monocytes from healthy children, perhaps a clue to the age dependency of COVID-19. These results suggest that the inflammatory malfunction in COVID-19 is rooted in the earliest perturbations that SARS-CoV-2 induces in epithelia. |Adult[MESH] |B-Lymphocytes/immunology[MESH] |COVID-19/*immunology/pathology[MESH] |Child[MESH] |Coculture Techniques[MESH] |Ebolavirus/pathogenicity[MESH] |Epithelial Cells/*immunology/virology[MESH] |Gene Expression Profiling[MESH] |Humans[MESH] |Inflammation[MESH] |Influenza A virus/pathogenicity[MESH] |Lung/immunology[MESH] |Monocytes/*immunology[MESH] |Myeloid Cells/immunology[MESH] |SARS-CoV-2/*pathogenicity[MESH] |Species Specificity[MESH]A virus-specific monocyte inflammatory phenotype is induced by SARS-Co(epmc).pdf DeepDyve Pubget Overpricing