Comparing the expression of MiR-223-NLRP3-IL-1β axis and serum IL-1β levels in patients with severe COVID-19 and healthy individuals

Abstract

Background and aimThe hyperactive nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a key factor for cytokine storm, chronic inflammation, and mortality in infected patients. On the subject of the regulation of the NLRP3-inflammasome activation, micro-ribonucleic acid (RNA)-223 (miR-223), among the major RNA molecules, has been thus far investigated in some inflammatory diseases along with interleukin-1 beta (IL-1β) and NLRP3. Against this background, the present study aimed to compare healthy individuals and patients with severe COVID-19 with reference to the alterations in the expression of the miR-223, NLRP3, and IL-1β axis and the serum IL-1β levels. MethodsIn total, 40 patients with severe COVID-19, admitted to the Infectious Ward of Razi Hospital, Ahvaz, Iran, who were homogenous in terms of age (40 years old) and gender, were selected based on the inclusion and exclusion criteria. The real-time polymerase chain reaction (RT-PCR) technique was then applied to assess the expression of the miR-223, NLRP3, and IL-1β genes, and enzyme-linked immunosorbent assay (ELISA) was then utilized to evaluate the serum IL-1β levels, using patients’ blood samples. Moreover, inflammatory biochemical markers of the participants were collected and recorded ResultsAccording to the study results, the IL-1β expression was 3.9 times higher in the patients with COVID-19, compared with the control group (p = 0.0005). The NLRP3 expression was also 6.04 times greater in the infected patients, compared with the healthy individuals (p < 0.0001). On the other hand, the miR-223 expression was 5.37 times lower in the case group, compared with the controls (p = 0.04). ConclusionThe study findings indicated the potential role of miR-223 and the dysregulation of NLRP3 inflammasome followed by IL-1β, as a regulatory factor in the pathogenesis of COVID-19, like that in other inflammatory diseases.