Abstracts Category : Other

Influence of human anti-mannan IgG subclass variants and complement on phagocytosis of Candida albicans

by Kaitlin Morgan

<i>Candida albicans</i> is one of the most common causes of nosocomial infection that can lead to serious or even fatal illness. <i> C. albicans</i> is naturally resistant to complement activation through its cell-surface displayed mannan, but the resistance can be overcome by anti-mannan antibody. Previous studies have shown that phagocytosis of <i>C. albicans </i> by human neutrophils is promoted by anti-mannan antibody but is not further enhanced by complement. The purpose of this study was to expand the previous study to include human macrophages and mouse neutrophils. First, human macrophages, derived from peripheral blood monocytes, were incubated with <i>C. albicans</i> in the presence of each of the four anti-mannan IgG antibodies (M1g1, M1g2, M1g3, and M1g4) with or without complement. Phagocytosis was determined by microscopy and phagocytic killing by colony forming unit. It was found that each variant had a subclass-specific effect to enhance both phagocytosis and phagocytic killing when compared to no-antibody control (p < 0.001) but addition of complement did not show a synergistic effect. Next, the effect of anti-mannan antibody and complement on phagocytosis of <i> C. albicans</i> by mouse neutrophil-like cells (MPRO) was assessed and results similar to those found with human macrophages were observed. Finally, an alternative method to determine phagocytic killing of <i>C. albicans </i> by human neutrophils was evaluated where respiratory burst values were measured in the presence of anti-mannan antibody and complement. It was found that respiratory burst was highly correlated with phagocytic killing based on colony forming unit (R = 0.652), but the correlation was not statistically significant (p = 0.077). Taken together, these results demonstrate that anti-mannan antibody is required for efficient phagocytosis and phagocytic killing of <i> C. albicans</i> and complement does not appear to enhance antibody-mediated phagocytosis.