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Up-regulation of IL-6 and TNF-α induced by SARS-coronavirus spike protein in murine macrophages via NF-κB pathway

Content Provider	Semantic Scholar
Author	Wang, Wei Ye, Linbai Li, Baozong Zeng, Yingchun Kong, Lingbao Fang, Xiaonan Zheng, Yuan Wu, Zhenghui She, Yinglong
Copyright Year	2007
Abstract	Abstract The clinical picture of severe acute respiratory syndrome (SARS) is characterized by an over-exuberant immune response with lung lymphomononuclear cells infilteration and proliferation that may account for tissue damage more than the direct effect of viral replication. To understand how cells response in the early stage of virus–host cell interaction, in this study, a purified recombinant S protein was studied for stimulating murine macrophages (RAW264.7) to produce proinflammatory cytokines (IL-6 and TNF-α) and chemokine IL-8. We found that direct induction of IL-6 and TNF-α release in the supernatant in a dose-, time-dependent manner and highly spike protein-specific, but no induction of IL-8 was detected. Further experiments showed that IL-6 and TNF-α production were dependent on NF-κB, which was activated through I-κBα degradation. These results suggest that SARS-CoV spike protein may play an important role in the pathogenesis of SARS, especially in inflammation and high fever.
Starting Page	1
Ending Page	8
Page Count	8
File Format	PDF HTM / HTML
DOI	10.1016/j.virusres.2007.02.007
PubMed reference number	17532082
Journal	Medline
Volume Number	128
Alternate Webpage(s)	https://ipfs.io/ipfs/bafykbzaced4xstofs4tc5q4irede6uzaz3qzcdvcb2eedxgfakzwdyjnxgohq/pdfs/2007%20Up-regulation%20of%20IL-6%20and%20TNF-_%20induced%20by%20SARS-coronavirus%20spike%20protein%20in%20murine%20macrophages%20via%20NF-_B%20pathway.pdf
Alternate Webpage(s)	https://api.elsevier.com/content/article/pii/S0168170207000470
Alternate Webpage(s)	https://www.sciencedirect.com/science/article/pii/S0168170207000470
Alternate Webpage(s)	https://doi.org/10.1016/j.virusres.2007.02.007
Journal	Virus Research
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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