Coronavirus Disease 2019 (COVID-19) caused by severe acute respiratory syndrome
coronavirus 2 (SARS-CoV-2) is a viral infection that results in respiratory disease,
which can evolve into multiorgan failure (MOF), leading to death (Aida A Abdelmaksoud et
al., 2021).

The first cases of COVID-19 were detected in Wuhan, China, in 2019. Since then, the
illness has spread rapidly around the country and the world reaching a pandemic level
(Rocklöv J et al., 2020). Cases have been reported in more than 180 countries to the
World Health Organization (WHO), including more than two million deaths (WHO, 2021).

Several biochemical alterations have been described in COVID-19 patients as lymphopenia,
thrombocytopenia and increased levels of C-reactive protein. The hallmark of severe
COVID-19 is the cytokine storm accompanied by a hyperinflammatory response in the host
due to the release of large amounts of pro-inflammatory cytokines IL-1β, IL-6, IL-2,
IL-7, TNF-α, interferon-γ (IFN)-γ, CRP, procalcitonin (PCT), lactate dehydrogenase (LDH),
erythrocyte sedimentation rate (ESR) and ferritin (Marcello Ciaccio and Agnello, 2020;
Shah A., 2020).

The inflammasome is a multiprotein complex, known for its role in the innate immune
response against viral diseases and a regulator of processing of the pro-inflammatory
cytokines interleukin (IL)-1β and IL-18. Inflammasome contains a NOD-like receptor (NLR)
sensor protein and pyrin domain-containing 3 , after which, NLRP3 Inflammasome was named
(de Rivero Vaccari et al., 2020). The presence of inflammasome-derived products such as
IL-1β, IL-18, and LDH in patients' sera suggests inflammasome engagement (Chen G et al.,
2020).

Increased IL-6, IL-10, and IL-4 were found in patients when compared with controls,
indicating that SARS-CoV-2 infects human monocytes and triggers NLRP3 inflammasome
activation. However, the definitive demonstration of NRLP3 inflammasome participation is
still required because these products can be produced via inflammasome-independent
pathways (Rodrigues et al., 2021). But, the possible contribution of NLRP3 inflammasome
activation and their ability to induce IL-1β production is still not clear .

The pronounced inflammatory characteristics of COVID-19 prompted us to investigate the
expression of the NRLP3 inflammasome and its relation to IL-1B in disease development and
severity and to determine the best anti-inflammatory will be used in COVID-19.