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SARS-CoV-2 infection induces a pro-inflammatory cytokine response through cGAS-STING and NF-kappaB #MMPMID35022513
Neufeldt CJ; Cerikan B; Cortese M; Frankish J; Lee JY; Plociennikowska A; Heigwer F; Prasad V; Joecks S; Burkart SS; Zander DY; Subramanian B; Gimi R; Padmanabhan S; Iyer R; Gendarme M; El Debs B; Halama N; Merle U; Boutros M; Binder M; Bartenschlager R
Commun Biol 2022[Jan]; 5 (1): 45 PMID35022513show ga
SARS-CoV-2 is a novel virus that has rapidly spread, causing a global pandemic. In the majority of infected patients, SARS-CoV-2 leads to mild disease; however, in a significant proportion of infections, individuals develop severe symptoms that can lead to long-lasting lung damage or death. These severe cases are often associated with high levels of pro-inflammatory cytokines and low antiviral responses, which can cause systemic complications. Here, we have evaluated transcriptional and cytokine secretion profiles and detected a distinct upregulation of inflammatory cytokines in infected cell cultures and samples taken from infected patients. Building on these observations, we found a specific activation of NF-kappaB and a block of IRF3 nuclear translocation in SARS-CoV-2 infected cells. This NF-kappaB response was mediated by cGAS-STING activation and could be attenuated through several STING-targeting drugs. Our results show that SARS-CoV-2 directs a cGAS-STING mediated, NF-kappaB-driven inflammatory immune response in human epithelial cells that likely contributes to inflammatory responses seen in patients and could be therapeutically targeted to suppress severe disease symptoms.
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Commun+Biol 2022 ; 5 (1): 45
