| Abstract [eng] |
The global COVID-19 pandemic in 2019 was caused by a severe acute respiratory syndrome virus known as coronavirus 2 (SARS-CoV-2). This virus is airborne and infects human respiratory cells. SARS-CoV-2 normally manifests itself as a common cold, but sometimes causes severe pneumonia, which is responsible for the high mortality rate. The aim of this thesis is to investigate whether SARS-CoV-2 S protein induces inflammation in macrophage-like cells. Objectives: To assess the secretion of the chemokine CXCL8 in THP-1 macrophages; to determine whether SARS-CoV-2 S protein induces the secretion of inflammatory molecules in THP-1 macrophages; and to determine whether SARS-CoV-2 S protein is phagocytosed by macrophage-like cells; to investigate the expression of the chemokine receptor CCR5 on the surface of macrophage cells using flow cytometry and to determine whether SARS-CoV-2 S protein and its complexes with antibodies, known as immune complexes, are incorporated into THP-1 macrophages. The inflammatory properties of SARS-CoV-2 S protein were investigated using the THP-1 human leukaemia monocytic cell line. Due to the different results reported in the scientific papers, the study aimed to determine the secretion of inflammatory molecules, the release of LDH and the cellular delivery of the S protein using fluorescence microscopy and flow cytometry. The results showed that SARS-CoV-2 S protein THP-1 does not induce secretion of inflammatory molecules, does not enter cells and is not phagocytosed in macrophage-like cells. |
