High efficiency opsonin-independent phagocytosis of Candida parapsilosis by human neutrophils.
Candida species are associated with invasive fungal infections, and C. parapsilosis has become increasingly prevalent. As key antifungal effector cells, the function of human neutrophils confronting C. parapsilosis was investigated. We hypothesized that interaction between neutrophils and Candida species may not be uniform. Opsonins were omitted from these studies to understand the antifungal mechanisms at their most basic level. Human neutrophils underwent phagocytosis of C. parapsilosis with much higher efficiency than with C. albicans. Immunofluorescence assays with ss-glucan specific antibody detected more surface exposed ss-glucan on C. parapsilosis than C. albicans. However, blockade of the ss-glucan receptor Dectin-1, reduced phagocytosis of C. albicans but not C. parapsilosis. Inclusion of excess beta-glucan, mannan, or chitin also had no effect on phagocytosis of C. parapsilosis. Consistent with the differences noted in phagocytosis, neutrophils mediated damage to C. parapsilosis but not C. albicans in assays of residual metabolic activity. C. parapsilosis was more sensitive to oxidative stress, and inclusion of antioxidant in toxicity assays decreased neutrophil mediated damage, suggesting that generation of reactive oxygen species contributes to the toxicity mechanism. These data suggest that the interaction between neutrophils and Candida species is not uniform and may partially account for differences observed in the epidemiology and natural history of infections caused by these species.
Linden
Jennifer R
JR
Graduate Program in Pathobiology, Brown University, Providence, RI 02905, USA.
Maccani
Matthew A
MA
Laforce-Nesbitt
Sonia S
SS
Bliss
Joseph M
JM
D000704:Analysis of Variance; D002175:Candida / Q000276:immunology* / Q000378:metabolism; D002686:Chitin / Q000378:metabolism; D015638:Cytochalasin D / Q000494:pharmacology; D005434:Flow Cytometry; D019084:Fluorescent Antibody Technique, Indirect; D054884:Host-Pathogen Interactions; D006801:Humans; D037181:Lectins, C-Type; D008351:Mannans / Q000378:metabolism; D008565:Membrane Proteins / Q000378:metabolism; D050296:Microbial Viability / Q000187:drug effects; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009504:Neutrophils / Q000276:immunology*; D010084:Oxidation-Reduction; D010587:Phagocytosis; D047071:beta-Glucans / Q000378:metabolism; D000099181:Dectin-1
D002686:Chitin; D015638:Cytochalasin D; D037181:Lectins, C-Type; D008351:Mannans; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; D047071:beta-Glucans; D000099181:Dectin-1