Deletion of Galectin-3 Renders Mice Less Susceptible to Candida auris Skin Infection by Enhancing Antifungal Activity of Neutrophils.

Candida auris is an emerging multidrug-resistant fungal pathogen that uniquely colonizes the skin. The factors regulating C auris colonization are poorly understood. In this study, we examined the role of galectin-3 during C auris skin infection. We found that deletion of galectin-3 enhances the antifungal activity of neutrophils and increases resistance to C auris skin infection. Mechanistically, galectin-3 negatively regulates GLUT4 expression, glucose uptake, reactive oxygen species production, and fungal killing by neutrophils. Collectively, our findings uncover a detrimental role for galectin-3 in neutrophil-mediated defense against C auris.