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BioMed Research International
Volume 2015, Article ID 398045, 13 pages
Research Article

The Absence of N-Acetyl-D-glucosamine Causes Attenuation of Virulence of Candida albicans upon Interaction with Vaginal Epithelial Cells In Vitro

1Department of Dermatology and Allergology, University of Szeged, Szeged, Hungary
2MTA-SZTE Dermatological Research Group, Hungary
3Institute of Biophysics, Biological Research Centre of the Hungarian Academy of Sciences, Szeged, Hungary
4Institute of Biochemistry, Biological Research Centre of the Hungarian Academy of Sciences, Szeged, Hungary
5Creative Laboratory Ltd., Szeged, Hungary

Received 19 May 2015; Revised 15 June 2015; Accepted 28 July 2015

Academic Editor: Stanley Brul

Copyright © 2015 Máté Manczinger et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


To better understand the molecular events underlying vulvovaginal candidiasis, we established an in vitro system. Immortalized vaginal epithelial cells were infected with live, yeast form C. albicans and C. albicans cultured in the same medium without vaginal epithelial cells were used as control. In both cases a yeast to hyphae transition was robustly induced. Whole transcriptome sequencing was used to identify specific gene expression changes in C. albicans. Numerous genes leading to a yeast to hyphae transition and hyphae specific genes were upregulated in the control hyphae and the hyphae in response to vaginal epithelial cells. Strikingly, the GlcNAc pathway was exclusively triggered by vaginal epithelial cells. Functional analysis in our in vitro system revealed that the GlcNAc biosynthesis is involved in the adherence to, and the ability to kill, vaginal epithelial cells in vitro, thus indicating the key role for this pathway in the virulence of C. albicans upon vulvovaginal candidiasis.