Fig. 7
From: Galectin-3 impacts Cryptococcus neoformans infection through direct antifungal effects
Gal-3 disrupts C. neoformans extracellular vesicles. Temporal kinetics of vesicle disruption mediated by Gal-3 were measured by dynamic light scattering over ten 30 s to read the population average size (a−c). The addition of Gal-3 10 μg initially leads to disruption (a). The same samples were read first without (blue line) and then with the presence of Gal-3 (red line), which was added between the 60 and 90 s intervals (red arrow). Hemocyanin, ovalbumin, concanavalin A (Con A), phytohaemagglutinin E (PHA-E), and phytohaemagglutinin L (PHA-L) were used as control (b). Also denatured Gal-3 and Gal-3 pre-incubated with lactosamine were used as control (c). Purified radiolabeled vesicles after 72 h post [1-14C] palmitic acid addition were resuspended in PBS, BSA, Gal-3 (0.001 to 10 μg/ml) (d), hemocyanin, ovalbumin, Con A, PHA-E, and PHA-L (e), denatured Gal-3 and Gal-3 pre-incubated with lactosamine (f), and supernatant (blue bars) and pellet (red bars) radioactivity were assessed and normalized to 100% radioactivity for each individual sample. Bars represent the mean ± SD from triplicate samples. Statistically significant differences are denoted by asterisks (*p < 0.05, **p < 0.005, unpaired Student’s t-test)
