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Activation of C-type lectin receptor and (RIG)-I-like receptors contributes to proinflammatory response in MERS coronavirus infected macrophages

Activation of C-type lectin receptor and (RIG)-I-like receptors contributes to proinflammatory response in MERS coronavirus infected macrophages

Journal of Infectious Diseases 2019

Human infection with Middle East respiratory syndrome coronavirus (MERS-CoV) poses an ongoing threat to public health worldwide. The studies of MERS patients with severe disease and experimentally-infected animals showed that robust viral replication and intensive proinflammatory response in lung tissues contribute to high pathogenicity of MERS-CoV. We sought to identify pattern recognition receptor (PRR) signaling pathway(s) that mediates the inflammatory cascade in human macrophages upon MERS-CoV infection. The potential signaling pathways were manipulated individually by pharmacological inhibition, siRNA depletion and antibody blocking. MERS-CoV-induced proinflammatory response was evaluated by measuring the expression levels of key cytokines/chemokines. RT-qPCR assay, flow cytometry analysis and Western blotting were applied to evaluate the activation of related PRRs and engagement of adaptors. MERS-CoV replication significantly upregulated C-type lectin receptor (CLR) Mincle. The role of Mincle for MERS-CoV-triggered cytokine/chemokine induction was established based on the results of antibody blockage, siRNA depletion of Mincle and its adaptor Syk, and Syk pharmacological inhibition. The cytokine/chemokine induction was significantly attenuated by siRNA depletion of RIG-I-like receptors (RLR) or adaptor, indicating RLR signaling also contributed to MERS-CoV-induced proinflammatory response. CLR and RLR pathways are activated and contribute to the proinflammatory response in MERS-CoV-infected macrophages.

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Accession: 069375007

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PMID: 31562757

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