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).