Abstract
Oral epithelial cells are the first cells that interact with C. albicans during the establishment of oropharyngeal candidiasis. Following initial adhesion, C. albicans invades oral epithelial cells by inducing its own endocytosis and gains access to epithelial vacuolar compartments. Epithelial endocytic pathways are key innate immune mechanisms in host defense. We examined the trafficking of C. albicans through oral epithelial endocytic compartments. We present evidence that C. albicans is internalized by oral epithelial cells through actin-dependent clathrin-mediated endocytosis and is taken into vacuolar compartments immediately following its internalization. C. albicans-containing endosomes transiently acquired early endosomal marker EEA1, but showed marked defects in acquisition of late endosomal marker LAMP1 and lysosomal marker cathepsin D. Defective endolysosomal maturation may partially explain the inability of oral epithelial cells to kill C. albicans.
Acknowledgements
This project was supported by Award # UL 1RR025767 from the National Center for Research Resources to CC Villar.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this paper.
This paper was first published online on Early Online on 24 September 2010.