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. 2020 Dec 2;2020:8829674. doi: 10.1155/2020/8829674

Figure 1.

Figure 1

The interaction hypothesis between neutrophil and hyperinflammation in COVID-19. After the host-viral interaction, the virus signaling leads to a cascade of interactions between the virus recognition mechanism, neutrophil activation, and inflammatory stimuli. The NETosis process can protect the host during the virus response or exacerbate lung hyperinflammation in COVID-19 patients. The figure is made with BioRender (https://app.biorender.com/). Abbreviations: SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; PAMP: pathogen-associated molecular pattern; DAMP: danger-associated molecular pattern; TNF: tumor necrosis factor; IL-6: interleukin-6; IL-1: interleukin-1; IL-8: interleukin-8; ROS: reactive oxygen species; NE: neutrophil elastase; MPO: myeloperoxidase.