A group from Washington State University, USA, etc. has reported that SARS-CoV-2 Spike is a key inducing proinflammatory response of macrophages.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8219098/
Virus replication and release of infectious progeny was determined by TCID50 assay in supernatants from SARS-CoV-2 infected Vero E6 cells and THP-1 human-derived macrophage-like cells as shown below. While THP-1 macrophages did not support productive SARS-CoV-2 replication, Vero E6 cells effectively replicated SARS-CoV-2.
To clarify the role of SARS-CoV-2 Spike in proinflammatory responses in macrophages, expression of the pro-inflammatory cytokines TNF-α, CXCL10 and IFN-γ and the antiviral cytokine IFN-β were evaluated with using THP-1. While Spike did not induce gene expression of antiviral IFN-β or IFN-γ in THP-1 macrophages, expression of proinflammatory TNF-α and CXCL10 was upregulated. TNF-α was upregulated by 30-fold at 4h post treatment with Spike (p < 0.05) and remained upregulated by two-fold at 16h post treatment. CXCL10 expression was consistently upregulated by 3 to 8-fold in THP-1 macrophages exposed to Spike up to 16h post treatment (p<0.05).