Prostaglandins and non-steroidal anti-inflammatory drugs in Covid-19.

ABSTRACT

In response to different viral infections, including SARS-CoV-2 infection, pro-inflammatory, anti-inflammatory cytokines, and bioactive lipids are released from infected and immune cells. One of the most critical bioactive lipids is prostaglandins (PGs) which favor perseverance of inflammation leading to chronic inflammation as PGs act as cytokine amplifiers. PGs trigger the release of pro-inflammatory cytokines, activate Th cells, recruit immune cells, and increase the expression of pro-inflammatory genes. Therefore, PGs may induce acute and chronic inflammations in various inflammatory disorders and viral infections like SARS-CoV-2. PGs are mainly inhibited by non-steroidal anti-inflammatory drugs (NSAIDs) by blocking cyclooxygenase enzymes (COXs), which involve PG synthesis. NSAIDs reduce inflammation by selective or non-selective blocking activity of COX2 or COX1/2, respectively. In the Covid-19 era, there is a tremendous controversy regarding the use of NSAIDs in the management of SARS-CoV-2 infection. As well, the possible role of PGs in the pathogenesis of SARS-CoV-2 infection is not well-defined. Thus, the objective of the present study is to review the potential role of PGs and NSAIDs in Covid-19 in a narrative review regarding the preponderance of assorted views.