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10.1002/JLB.5COVBCR0720-310RR

http://scihub22266oqcxt.onion/10.1002/JLB.5COVBCR0720-310RR
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32794348!7436862!32794348
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suck abstract from ncbi


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pmid32794348      J+Leukoc+Biol 2021 ; 109 (1): 115-120
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  • Mismatch between circulating cytokines and spontaneous cytokine production by leukocytes in hyperinflammatory COVID-19 #MMPMID32794348
  • Kahn R; Schmidt T; Golestani K; Mossberg A; Gullstrand B; Bengtsson AA; Kahn F
  • J Leukoc Biol 2021[Jan]; 109 (1): 115-120 PMID32794348show ga
  • The disease COVID-19 has developed into a worldwide pandemic. Hyperinflammation and high levels of several cytokines, for example, IL-6, are observed in severe COVID-19 cases. However, little is known about the cellular origin of these cytokines. Here, we investigated whether circulating leukocytes from patients with COVID-19 had spontaneous cytokine production. Patients with hyperinflammatory COVID-19 (n = 6) and sepsis (n = 3) were included at Skane University Hospital, Sweden. Healthy controls were also recruited (n = 5). Cytokines were measured in COVID-19 and sepsis patients using an Immulite immunoassay system. PBMCs were cultured with brefeldin A to allow cytokine accumulation. In parallel, LPS was used as an activator. Cells were analyzed for cytokines and surface markers by flow cytometry. High levels of IL-6 and measurable levels of IL-8 and TNF, but not IL-1beta, were observed in COVID-19 patients. Monocytes from COVID-19 patients had spontaneous production of IL-1beta and IL-8 (P = 0.0043), but not of TNF and IL-6, compared to controls. No spontaneous cytokine production was seen in lymphocytes from either patients or controls. Activation with LPS resulted in massive cytokine production by monocytes from COVID-19 patients and healthy controls, but not from sepsis patients. Finally, monocytes from COVID-19 patients produced more IL-1beta than from healthy controls (P = 0.0087) when activated. In conclusion, monocytes contribute partly to the ongoing hyperinflammation by production of IL-1beta and IL-8. Additionally, they are responsive to further activation. This data supports the notion of IL-1beta blockade in treatment of COVID-19. However, the source of the high levels of IL-6 remains to be determined.
  • |Aged[MESH]
  • |Aged, 80 and over[MESH]
  • |COVID-19/*immunology/pathology[MESH]
  • |Cytokines/*immunology[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Monocytes/*immunology/pathology[MESH]


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