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Published on: June 27, 2011
Galectin-3 binding protein stimulated IL-6 expression is impeded by antibody intervention in SARS-CoV-2 susceptible
Ana Mendes-Frias1,2, Valentina Gallo3,4, Valentina Iacobelli5
1Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, 4710-057, Braga, Portugal.
Abstract:
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.
Insights
Galectin-3 binding protein (Gal-3BP) fragment D2 stimulates IL-6 production in epithelial cells. An antibody targeting Gal-3BP can block this effect, suggesting a therapeutic strategy for severe COVID-19 and cytokine storm.
Area of Science:
- Immunology
- Molecular Biology
- Virology
Background:
- COVID-19 pandemic necessitates understanding severe disease mechanisms.
- Galectin-3 (Gal-3) and its binding protein (Gal-3BP) are implicated in COVID-19 severity.
- Gal-3BP activation links to pro-inflammatory cytokine production and cytokine storm (CS).
Purpose of the Study:
- To investigate the role of Gal-3BP in IL-6 induction in epithelial cells.
- To evaluate the therapeutic potential of targeting Gal-3BP in COVID-19.
Main Methods:
- Utilized a recombinant Gal-3BP fragment (D2) to stimulate IL-6 expression in colon and lung epithelial cell lines.
- Assessed IL-6 induction in a β-galactoside dependent manner.
- Tested the efficacy of an anti-Gal-3BP monoclonal antibody (1959) in blocking D2-induced IL-6 production.
Main Results:
- D2 fragment significantly stimulated IL-6 expression in epithelial cells.
- IL-6 induction by D2 was dependent on β-galactoside binding.
- The anti-Gal-3BP antibody 1959 effectively reduced D2-induced IL-6 augmentation.
Conclusions:
- Gal-3BP activation contributes to IL-6 mediated inflammation in epithelial cells.
- Antibody-mediated blockade of Gal-3BP shows promise for preventing/treating cytokine storm in severe COVID-19.
