3.3 Neutrophils-mediated inflammation in COVID-19
With the continual reduction detected in lymphocytes count of COVID-19 patients, they become more prone for secondary infections with the risk of high mortality rate. This occurs due to loss of all lymphocyte effector cells that possess the essential antiviral activity, including CD8+ or cytotoxic lymphocytes and natural killer cells, as well as B cells, which able to form the specific antibodies targeted for inactivating the virus (Dallan et al., 2020; Remy et al., 2020).
Therefore, developing severe lymphopenia will effectively inhibit the stimulation of adaptive cell-mediated immune response and consequently, facilitate the inflammatory-mediated neutrophils response which could be started with their chemotaxis and recruitment, followed by degranulation (Hyun and Hong, 2017; Didangelos, 2020). Neutrophils possess an arsenal of proteases such as (elastase, proteinase-3 and cathepsin G), inflammatory mediators such as (TNF-α and IL-6), and toxic oxidants that do not kill phagocytosed pathogens only, but also can damage the host tissue (Gernez et al., 2010).