The Impacts of Anti-Inflammatory Agents on COVID-19 Cytokine Storm

The re-emergence of severe acute respiratory syndrome coronavirus 2 A(SARS-CoV-2) in Wuhan, China, has placed an unprecedented economic and health burden globally. The SARS-CoV-2 high mortality rate has brought great challenges to researchers, clinicians, and health workers in their bid to discover appropriate therapeutic interventions. The search for the ultimate remedy was initially centered on the use of antiviral agents targeting receptors and proteins involved in the pathophysiology of SARS-CoV-2. However, the upsurge of interest in repurposing anti-inflammatory agents was born out of the reported risks posed by a cytokine storm on COVID-19-induced fatality. A cytokine storm, as a result of the unregulated production of pro-inflammatory cytokines and other chemical mediators, triggers coagulopathy, viral sepsis, pneumonitis shock, and acute respiratory syndrome, which may lead directly to respiratory and organ failure and ultimately the death of the patient. The overwhelming evidence has shown that the early prediction of cytokine storm using serum chemistry and hematological markers and the use of appropriate anti-inflammatory agents will avert COVID-19 complications. These include the use of repurposed interferon (IFN) therapy and inhibitors of interleukin-1 (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and Janus kinase (JAKs) to nip the cytokine storm in the bud. This review critically used information retrieved from PubMed, China National Knowledge Infrastructure, Embase, Medline, and Google Scholar to elaborate on the mechanism and complications of COVID-19 cytokine storm, therapeutic interventions, and the way forward to discovering effective biocompatible drug targets.