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. 2020 Sep:159:105051.
doi: 10.1016/j.phrs.2020.105051. Epub 2020 Jun 27.

Targeting inflammation and cytokine storm in COVID-19

Qianwen Huang  1 , Xiumei Wu  1 , Xueying Zheng  2 , Sihui Luo  2 , Suowen Xu  3 , Jianping Weng  4
Affiliations

Targeting inflammation and cytokine storm in COVID-19

Qianwen Huang et al. Pharmacol Res. 2020 Sep.
No abstract available

PubMed Disclaimer

Conflict of interest statement

None declared.

Figures

Fig. 1
Fig. 1
Potential therapies of COVID-19 by targeting inflammation and cytokine storm. SARS-CoV-2 enters and infects cells by binding to TMPRSS2 and ACE2, subsequently releases virus RNA, one of the PAMPs, and recruits dendritic cells, macrophages and neutrophils. The released type I interferon and pro-inflammatory cytokines and chemokines induce the innate immune response while adaptive immune response is ignited by activating T and B lymphocytes to defend against the virus. Meanwhile, intact viruses or the components can directly activate the NLRP3 inflammasome, leading to IL-1β secretion. In most infections, moderate immune response and antiviral response are capable to combat the infection. Nevertheless, in individuals with immunological dysfunction, persistent hyper-inflammation triggers a cytokine storm, leading to the lung injury and ARDS or eventually swept through the whole body, causing MODS. During the pathological progression, the inhibition of NRLP3, JAK1/2, IL-6, BRD4 and the infusion of IVIG may be beneficial in suppressing the overwhelming inflammation and arrest or reverse the COVID-19 disease. Abbreviations: ACE2, angiotensin converting enzyme 2; ARDS, acute respiratory distress syndrome; IVIG, intravenous immunoglobulin; MODS, multiple organ dysfunction syndrome; NLRP3, Nod-like receptor protein 3; PAMP, pathogen-associated molecular pattern; TMPRSS2, transmembrane serine protease 2.
See this image and copyright information in PMC

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