Abstract
Recent in vitro studies have implicated galectin-3 as an important receptor in host recognition and response to specific Candida species; however, its role in protection against disseminated candidiasis in vivo has not been evaluated. This study investigated the importance of galectin-3 in host defense against systemic infection with the highly virulent species Candida albicans, and the less virulent species, C. parapsilosis. Mice deficient in galectin-3 (gal3−/−) were more susceptible to infection than wild-type (WT) mice. When infected with C. albicans, gal3−/− mice died significantly faster and exhibited a trend towards increased fungal burden and increased abscess formation in infected brains compared to WT mice. When infected with C. parapsilosis, gal3−/− mice had significantly higher renal fungal burdens and abscess formation compared to WT mice. To evaluate whether galectin-3 may contribute to susceptibility to candidiasis in human infants, galectin-3 levels in sera of newborn infants, a patient population uniquely susceptible to infections with both C. albicans and C. parapsilosis, were compared to serum galectin-3 levels of adults. Galectin-3 levels were significantly lower in newborn infant sera compared to adult sera. These data indicate that galectin-3 plays an important role in a murine model of disseminated candidiasis and suggest a potential mechanism of neonatal susceptibility to these infections.
Acknowledgements
Many thanks to Richard Tucker for assistance with statistical analysis and the Eunice Kennedy Shriver NICHD Neonatal Research Network for supplying clinical isolate 14-72391-101. This project was supported by grants from the National Center for Research Resources (5P20RR018728-10) and the National Institute of General Medical Sciences (8P20GM103537-10) from the National Institutes of Health.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and the writing of the paper.