Galectin-3 expression and effect of supplementation in neonatal mice with disseminated Candida albicans infection

Invasive candidiasis is an important cause of fungal infections in immunocompromised patients, including premature infants. The S-type lectin, galectin-3 (gal3), is increasingly recognized for its role in antifungal host defense. This study tested the hypothesis that tissue gal3 expression is affected by disseminated infection with Candida albicans and that supplementation with gal3 will provide a benefit in this setting.

To determine the expression of gal3 at the tissue level in response to disseminated infection with C. albicans, adult and neonatal mice were infected using previously established models. End points were chosen that reflected substantive tissue fungal burden but before mortality.

No differences in gal3 were detected in tissues of adult animals relative to uninfected controls. In neonatal animals, gal3 concentration was lower in the spleen of infected animals compared to uninfected. Pretreatment of neonatal mice with recombinant gal3 was associated with reduced mortality and reduced fungal burden in the kidney, spleen, and lung at 24 h following infection.

These findings suggest that gal3 has an active role in host defense against candidiasis and that neonatal animals can benefit from supplementation with this lectin in the setting of disseminated candidiasis.