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Mediators of Inflammation
Volume 2010 (2010), Article ID 940383, 13 pages
http://dx.doi.org/10.1155/2010/940383
Research Article

Normal Human Gingival Epithelial Cells Sense C. parapsilosis by Toll-Like Receptors and Module Its Pathogenesis through Antimicrobial Peptides and Proinflammatory Cytokines

1Groupe de Recherche en Écologie Buccale, Faculté de Médecine Dentaire, Pavillon de Médecine Dentaire, Université Laval, QC, Canada G1K 7P4
2Laboratoire d’Analyse, Traitement et Valorisation des Polluants de l’Environnement et des Produits, Faculté de Pharmacie, Rue Avicenne, 5019 Monastir, Tunisia

Received 2 December 2009; Revised 12 February 2010; Accepted 15 February 2010

Academic Editor: Kathy Triantafilou

Copyright © 2010 Raouf Bahri 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.

Abstract

This study was designed to investigate the interaction between C. parapsilosis and human epithelial cells using monolayer cultures and an engineered human oral mucosa (EHOM). C. parapsilosis was able to adhere to gingival epithelial cells and to adopt the hyphal form in the presence of serum. Interestingly, when cultured onto the engineered human oral mucosa (EHOM), C. parapsilosis formed small biofilm and invaded the connective tissue. Following contact with C. parapsilosis, normal human gingival epithelial cells expressed high levels of Toll-like receptors (TLR)-2, -4, and -6, but not TLR-9 mRNA. The upregulation of TLRs was paralleled by an increase of IL-1 , TNF , and IFN mRNA expression, suggesting the involvement of these cytokines in the defense against infection with C. parapsilosis. The active role of epithelial cells in the innate immunity against C. parapsilosis infection was enhanced by their capacity to express high levels of human beta-defensin-1, -2, and -3. The upregulation of proinflammatory cytokines and antimicrobial peptide expression may explain the growth inhibition of C. parapsilosis by the gingival epithelial cells. Overall results provide additional evidence of the involvement of epithelial cells in the innate immunity against C. parapsilosis infections.