Galectin-3 binding protein stimulated IL-6 expression is impeded by antibody intervention in SARS-CoV-2 susceptible cell lines

• Published in: Scientific reports Vol. 12; no. 1; p. 17047
• Main Authors: Mendes-Frias, Ana, Gallo, Valentina, Iacobelli, Valentina, Gentile, Roberta, Antonini, Giovanni, Silvestre, Ricardo, Iacobelli, Stefano
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 11.10.2022; Nature Publishing Group; Nature Portfolio
• Subjects: 631/154; 631/250; 631/45; 631/80; 692/308; 692/699; Antibodies; Antibodies, Monoclonal - metabolism; Antibodies, Monoclonal - pharmacology; Carrier Proteins; Cell Line; Cell lines; Cell surface; Coronaviruses; COVID-19; COVID-19 Drug Treatment; Cytokine Release Syndrome; Cytokine storm; Cytokines - metabolism; Epithelial cells; Galectin 3 - metabolism; Galectin-3; Humanities and Social Sciences; Humans; Inflammation; Interleukin 6; Interleukin-6 - metabolism; Monoclonal antibodies; multidisciplinary; Pandemics; Pathophysiology; Patients; SARS-CoV-2; Science; Science (multidisciplinary); Severe acute respiratory syndrome coronavirus 2; Therapeutic targets
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-022-20852-x

COVID-19 is the global pandemic that affected our population in the past 2 years. Considerable research has been done to better understand the pathophysiology of this disease and to identify new therapeutic targets, especially for severe cases. Galectin-3 (Gal-3) is a receptor present at the surface of different cell types, namely epithelial and inflammatory cells, which has been described as a severity marker in COVID-19. The activation of Gal-3 through its binding protein (Gal-3BP) is directly linked to the production of pro-inflammatory cytokines that contribute for the cytokine storm (CS) observed in severe COVID-19 patients. Here, we show that D2, a recombinant fragment of the lectin-binding region of Gal-3BP was able to stimulate the expression of IL-6 in colon and lung epithelial cell lines in β-galactoside dependent manner. We further show that D2-induced IL-6 augmentation was reduced by the anti-Gal-3BP monoclonal antibody 1959. Our data confirm and extend prior findings of Gal-3BP mediated IL-6 induction, enlightening the potential of its antibody-mediated s blockage for the prevention and treatment of CS and severe disease in COVID-19 patients.