Open AccessThe role of galectin‐3 in phagocytosis of C andida albicans and C andida parapsilosis by human neutrophils
Author(s) -
Linden Jennifer R.,
Kunkel Dennis,
LaforceNesbitt Sonia S.,
Bliss Joseph M.
Publication year - 2013
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12103
Subject(s) - candida albicans , phagocytosis , corpus albicans , microbiology and biotechnology , candida parapsilosis , biology , yeast , antibody opsonization , opsonin , biochemistry
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.