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10.21203/rs.3.rs-1083825/v1

http://scihub22266oqcxt.onion/10.21203/rs.3.rs-1083825/v1
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34845442!8629200!34845442
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suck abstract from ncbi


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pmid34845442      Res+Sq 2021 ; ä (ä): ä
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  • Severe COVID-19 infection is associated with aberrant cytokine production by infected lung epithelial cells rather than by systemic immune dysfunction #MMPMID34845442
  • Rouhani SJ; Trujillo JA; Pyzer AR; Yu J; Fessler J; Cabanov A; Higgs EF; Cron KR; Zha Y; Lu Y; Bloodworth JC; Abasiyanik MF; Okrah S; Flood BA; Hatogai K; Leung MY; Pezeshk A; Kozloff L; Reschke R; Strohbehn GW; Chervin CS; Kumar M; Schrantz S; Madariaga ML; Beavis KG; Yeo KJ; Sweis RF; Segal J; Tay S; Izumchenko E; Mueller J; Chen LS; Gajewski TF
  • Res Sq 2021[Nov]; ä (ä): ä PMID34845442show ga
  • The mechanisms explaining progression to severe COVID-19 remain poorly understood. It has been proposed that immune system dysregulation/over-stimulation may be implicated, but it is not clear how such processes would lead to respiratory failure. We performed comprehensive multiparameter immune monitoring in a tightly controlled cohort of 128 COVID-19 patients, and used the ratio of oxygen saturation to fraction of inspired oxygen (SpO2 / FiO2) as a physiologic measure of disease severity. Machine learning algorithms integrating 139 parameters identified IL-6 and CCL2 as two factors predictive of severe disease, consistent with the therapeutic benefit observed with anti-IL6-R antibody treatment. However, transcripts encoding these cytokines were not detected among circulating immune cells. Rather, in situ analysis of lung specimens using RNAscope and immunofluorescent staining revealed that elevated IL-6 and CCL2 were dominantly produced by infected lung type II pneumocytes. Severe disease was not associated with higher viral load, deficient antibody responses, or dysfunctional T cell responses. These results refine our understanding of severe COVID-19 pathophysiology, indicating that aberrant cytokine production by infected lung epithelial cells is a major driver of immunopathology. We propose that these factors cause local immune regulation towards the benefit of the virus.
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