Please use this identifier to cite or link to this item: http://repository.unizik.edu.ng/handle/123456789/536
Title: Targeting Specific Checkpoints in the Management of SARS-CoV-2 Induced Cytokine Storm
Authors: Abubakar, Abdullahi Rabiu
Ahmad, Rahnuma
Rowaiye, Adekunle Babajide
Rahman, Sayeeda
Iskandar, Katia
Dutta, Siddhartha
Oli, Angus Nnamdi
Dhingra, Sameer
Tor, Maryam Abba
Etando, Ayukafangha
Kumar, Santosh
Irfan, Mohammed
Gowere, Marshall
Chowdhury, Kona
Akter, Farhana
Jahan, Dilshad
Schellack, Natalie
Haque, Mainul
Keywords: cytokine storm
SARS-CoV-2
COVID-19
pathogenesis
immune response
interleukins
hyperinflammation
Issue Date: 25-Mar-2022
Publisher: Multidisciplinary Digital Publishing Institute
Citation: Life, 12, 478.
Abstract: COVID-19-infected patients require an intact immune system to suppress viral replication and prevent complications. However, the complications of SARS-CoV-2 infection that led to death were linked to the overproduction of proinflammatory cytokines known as cytokine storm syndrome. This article reported the various checkpoints targeted to manage the SARS-CoV-2-induced cytokine storm. The literature search was carried out using PubMed, Embase, MEDLINE, and China National Knowledge Infrastructure (CNKI) databases. Journal articles that discussed SARS-CoV-2 infection and cytokine storm were retrieved and appraised. Specific checkpoints identified in managing SARS-CoV-2 induced cytokine storm include a decrease in the level of Nod-Like Receptor 3 (NLRP3) inflammasome where drugs such as quercetin and anakinra were effective. Janus kinase-2 and signal transducer and activator of transcription-1 (JAK2/STAT1) signaling pathways were blocked by medicines such as tocilizumab, baricitinib, and quercetin. In addition, inhibition of interleukin (IL)-6 with dexamethasone, tocilizumab, and sarilumab effectively treats cytokine storm and significantlyreduces mortality caused by COVID-19. Blockade of IL-1 with drugs such as canakinumab and anakinra, and inhibition of Bruton tyrosine kinase (BTK) with zanubrutinib and ibrutinib was also beneficial. These agents' overall mechanisms of action involve a decrease in circulating proinflammatory chemokines and cytokines and or blockade of their receptors. Consequently, the actions of these drugs significantly improve respiration and raise lymphocyte count and PaO2/FiO 2ratio.Targeting cytokine storms' pathogenesis genetic and molecular apparatus will substantially enhance lung function and reduce mortality due to the COVID-19 pandemic.
Description: Scholarly Work
URI: https://doi.org/10.3390/life12040478
http://repository.unizik.edu.ng/handle/123456789/536
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