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  • Long-lived macrophage reprogramming drives spike protein-mediated inflammasome activation in COVID-19 #MMPMID34133077
  • Theobald SJ; Simonis A; Georgomanolis T; Kreer C; Zehner M; Eisfeld HS; Albert MC; Chhen J; Motameny S; Erger F; Fischer J; Malin JJ; Grab J; Winter S; Pouikli A; David F; Boll B; Koehler P; Vanshylla K; Gruell H; Suarez I; Hallek M; Fatkenheuer G; Jung N; Cornely OA; Lehmann C; Tessarz P; Altmuller J; Nurnberg P; Kashkar H; Klein F; Koch M; Rybniker J
  • EMBO Mol Med 2021[Aug]; 13 (8): e14150 PMID34133077show ga
  • Innate immunity triggers responsible for viral control or hyperinflammation in COVID-19 are largely unknown. Here we show that the SARS-CoV-2 spike protein (S-protein) primes inflammasome formation and release of mature interleukin-1beta (IL-1beta) in macrophages derived from COVID-19 patients but not in macrophages from healthy SARS-CoV-2 naive individuals. Furthermore, longitudinal analyses reveal robust S-protein-driven inflammasome activation in macrophages isolated from convalescent COVID-19 patients, which correlates with distinct epigenetic and gene expression signatures suggesting innate immune memory after recovery from COVID-19. Importantly, we show that S-protein-driven IL-1beta secretion from patient-derived macrophages requires non-specific monocyte pre-activation in vivo to trigger NLRP3-inflammasome signaling. Our findings reveal that SARS-CoV-2 infection causes profound and long-lived reprogramming of macrophages resulting in augmented immunogenicity of the SARS-CoV-2 S-protein, a major vaccine antigen and potent driver of adaptive and innate immune signaling.
  • |*COVID-19[MESH]
  • |*Spike Glycoprotein, Coronavirus[MESH]
  • |Humans[MESH]
  • |Immunity, Innate[MESH]
  • |Inflammasomes[MESH]
  • |Interleukin-1beta[MESH]
  • |Macrophages[MESH]
  • |NLR Family, Pyrin Domain-Containing 3 Protein/genetics[MESH]
  • |SARS-CoV-2[MESH]

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  • suck abstract from ncbi

    e14150 8.13 2021