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10.15252/embj.2021107826 http://scihub22266oqcxt.onion/10.15252/embj.2021107826 34101213!8209947!34101213     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+J 2021 ; 40 (15): e107826 Nephropedia Template TP {{tp|p=34101213|t=2021. SARS-CoV-2 sensing by RIG-I and MDA5 links epithelial infection to macrophage inflammation |pdf=|usr=}}{{34101213}} gab.com Text SARS-CoV-2 sensing by RIG-I and MDA5 links epithelial infection to macrophage inflammation JO: EMBO J http://www.kidney.de/pget.php?&tw=1&pmid=34101213 #FOAvip SARS-CoV-2 infection causes broad-spectrum immunopathological disease, exacerbated by inflammatory co-morbidities. A better understanding of mechanisms underpinning virus-associated inflammation is required to develop effective therapeutics. Here, we discover that SARS-CoV-2 replicates rapidly in lung epithelial cells despite triggering a robust innate immune response through the activation of cytoplasmic RNA sensors RIG-I and MDA5. The inflammatory mediators produced during epithelial cell infection can stimulate primary human macrophages to enhance cytokine production and drive cellular activation. Critically, this can be limited by abrogating RNA sensing or by inhibiting downstream signalling pathways. SARS-CoV-2 further exacerbates the local inflammatory environment when macrophages or epithelial cells are primed with exogenous inflammatory stimuli. We propose that RNA sensing of SARS-CoV-2 in lung epithelium is a key driver of inflammation, the extent of which is influenced by the inflammatory state of the local environment, and that specific inhibition of innate immune pathways may beneficially mitigate inflammation-associated COVID-19. Twit Text FOAVip SARS-CoV-2 sensing by RIG-I and MDA5 links epithelial infection to macrophage inflammation ????EMBO J http://www.kidney.de/pget.php?&tw=1&pmid=34101213 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34101213 #FOAvip English Wikipedia <ref>{{Cite pmid|34101213}}</ref> SARS-CoV-2 sensing by RIG-I and MDA5 links epithelial infection to macrophage inflammation #MMPMID34101213 Thorne LG; Reuschl AK; Zuliani-Alvarez L; Whelan MVX; Turner J; Noursadeghi M; Jolly C; Towers GJ EMBO J 2021[Aug]; 40 (15): e107826 PMID34101213show ga SARS-CoV-2 infection causes broad-spectrum immunopathological disease, exacerbated by inflammatory co-morbidities. A better understanding of mechanisms underpinning virus-associated inflammation is required to develop effective therapeutics. Here, we discover that SARS-CoV-2 replicates rapidly in lung epithelial cells despite triggering a robust innate immune response through the activation of cytoplasmic RNA sensors RIG-I and MDA5. The inflammatory mediators produced during epithelial cell infection can stimulate primary human macrophages to enhance cytokine production and drive cellular activation. Critically, this can be limited by abrogating RNA sensing or by inhibiting downstream signalling pathways. SARS-CoV-2 further exacerbates the local inflammatory environment when macrophages or epithelial cells are primed with exogenous inflammatory stimuli. We propose that RNA sensing of SARS-CoV-2 in lung epithelium is a key driver of inflammation, the extent of which is influenced by the inflammatory state of the local environment, and that specific inhibition of innate immune pathways may beneficially mitigate inflammation-associated COVID-19. |*SARS-CoV-2/genetics/physiology[MESH] |COVID-19/genetics/*immunology/virology[MESH] |Cell Line[MESH] |Cytokines/genetics/immunology[MESH] |DEAD Box Protein 58/*immunology[MESH] |Epithelial Cells/*immunology/virology[MESH] |Host-Pathogen Interactions[MESH] |Humans[MESH] |Immunity, Innate[MESH] |Inflammation/genetics/immunology/virology[MESH] |Interferon-Induced Helicase, IFIH1/*immunology[MESH] |Janus Kinases/immunology[MESH] |Lung/cytology/immunology/virology[MESH] |Macrophage Activation[MESH] |Macrophages/*immunology[MESH] |NF-kappa B/immunology[MESH] |RNA, Viral/*immunology[MESH] |Receptors, Immunologic/*immunology[MESH] |Respiratory Mucosa/cytology/immunology/virology[MESH] |STAT Transcription Factors/immunology[MESH]SARS-CoV-2 sensing by RIG-I and MDA5 links epithelial infection to mac(epmc).pdf DeepDyve Pubget Overpricing