Fig 2: Gal-3 displays a more potent proinflammatory profile than Gal-8 and Gal-9. (A) Correlation of IL-6 with Gal-3 levels in the plasma of the Wuhan cohort. (B) Correlation of TNF-α with Gal-3 in the Wuhan cohort. (C) Correlation of GM-CSF with Gal-9 in the Wuhan cohort. (D) Correlation of MDC with Gal-3 in the Wuhan cohort. (E) Correlation of IL-8 with Gal-3 in the Wuhan cohort. (F) Correlation of IL-6 with Gal-3 levels in the Delta cohort. (G) Correlation of TNF-α with Gal-3 in the Delta cohort. (H) Correlation of MCP-1 with Gal-3 in the Delta cohort. (I) Detected concentrations of IL-6 in culture supernatants of treated PBMCs from SARS-CoV-2 uninfected individuals with rhGal-3 (0.02 µg/mL), rhGal-8 (0.02 µg/mL), and rhGal-9 (0.02 µg/mL) for overnight as quantified by ELISA. (J) Detected concentrations of TNF-α in culture supernatants of treated PBMCs from SARS-CoV-2-uninfected individuals with rhGal-3 (0.02 µg/mL), rhGal-8 (0.02 µg/mL), and rhGal-9 (0.02 µg/mL) for overnight as quantified by ELISA. (K) Representative flow cytometry plots and cumulative data of percentages of (L) TNF-α and (M) IL-6 expressing monocytes (CD14) in treated PBMCs from SARS-CoV-2-uninfected individuals following treatment with rhGal-3 (0.02 µg/mL), rhGal-8 (0.02 µg/mL), and rhGal-9 (0.02 µg/mL) and their combination for 6 h as measured by ICS. The LPS (2 µg/mL) was used as a positive control. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.