The role of galectin‐3 in phagocytosis of C andida albicans and C andida parapsilosis by human neutrophils

Summary C andida albicans causes the majority of invasive candidiasis in immunocompromised adults while C andida parapsilosis is a leading cause of neonatal candidiasis. While much work has focused on how the immune system recognizes and responds to C . albicans , less is known about host interaction with C . parapsilosis . This study investigates the human neutrophil phagocytic response to these species. Neutrophils underwent phagocytosis of C . parapsilosis yeast and C . albicans hyphae much more efficiently than C . albicans yeast. Treatment of neutrophils with a galectin‐3 (gal3) blocking antibody inhibited phagocytosis of C . parapsilosis yeast and C . albicans hyphae, but not C . albicans yeast. The majority of neutrophil gal3 was expressed intracellularly and was secreted from neutrophils after treatment with C . parapsilosis mannan. When neutrophils were treated with exogenous gal3, phagocytosis of both C . albicans and C . parapsilosis yeast increased. Exposure of neutrophils to C . parapsilosis yeast increased phagocytosis of C . albicans yeast and was inhibited by gal3 blocking antibody. Taken together, these data indicate that gal3 secreted from neutrophils may act as a pro‐inflammatory autocrine/paracrine signal in neutrophil phagocytosis and suggest that gal3 has a unique role in neutrophil response to C . parapsilosis yeast and C . albicans hyphae distinct from C . albicans yeast.