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Regulation of TLR8-activated gene expression in human neutrophils [RNA-seq neutrophils & monocytes]

ABSTRACT: Regulation of TLR8-activated gene expression in human neutrophils [RNA-seq neutrophils & monocytes]

PROVIDER: PRJNA489111 | ENA |

REPOSITORIES: ENA

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Regulation of TLR8-activated gene expression in human neutrophils

Project description:Regulation of TLR8-activated gene expression in human neutrophils

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Regulation of TLR8-activated gene expression in human neutrophils [RNA-seq neutrophils & monocytes]

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SARS-CoV-2-associated ssRNAs activate human neutrophils in a TLR8-dependent fashion

Project description:COVID-19 disease is characterized by a dysregulation of the innate arm of the immune system. However, the mechanisms whereby innate immune cells, including neutrophils, become activated in patients are not completely understood. Recently, we showed that a GU-rich RNA sequence from SARS-CoV-2 genome (i.e., SCV2-RNA2) activates dendritic cells. To clarify whether human neutrophils may also represent targets of SCV2-RNA2, neutrophils were treated with either SCV2-RNA2 or, as control, R848 (a TLR7/8 ligand), and then analysed for several functional assays and also subjected to RNA-seq experiments. Results highlight a remarkable response of neutrophils to SCV2-RNA2 in terms of TNFa, IL1ra, CXCL8 production, apoptosis delay, modulation of CD11b and CD62L expression and release of neutrophil extracellular traps. By RNA-seq experiments, we observed that SCV2-RNA2 promotes a transcriptional reprogramming of neutrophils, characterized by the induction of thousands of proinflammatory genes, similarly to that promoted by R848. Furthermore, by using CU-CPT9a, a TLR8-specific inhibitor, we found that SCV2-RNA2 stimulates neutrophils exclusively via TLR8-dependent pathways. In sum, our study proves that single-strand RNAs from the SARS-CoV-2 genome potently activate human neutrophils via TLR8, thus uncovering a potential mechanism whereby neutrophils may contribute to the pathogenesis of severe COVID-19 disease.

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