Molecular and Cellular Mechanisms That Lead to Candida Biofilm Formation

Author:

ten Cate J.M.123,Klis F.M.123,Pereira-Cenci T.123,Crielaard W.123,de Groot P.W.J.123

Affiliation:

1. Department of Cariology Endodontology Pedodontology, Academic Centre for Dentistry Amsterdam -ACTA-, University of Amsterdam and Free University Amsterdam, Louwesweg 1, 1066 EA Amsterdam, the Netherlands;

2. Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, the Netherlands; and

3. Department of Prosthodontics and Periodontology, Faculty of Dentistry of Piracicaba, UNICAMP, Brazil

Abstract

Fungal infections in the oral cavity are mainly caused by C. albicans, but other Candida species are also frequently identified. They are increasing in prevalence, especially in denture-wearers and aging people, and may lead to invasive infections, which have a high mortality rate. Attachment to mucosal tissues and to abiotic surfaces and the formation of biofilms are crucial steps for Candida survival and proliferation in the oral cavity. Candida species possess a wide arsenal of glycoproteins located at the exterior side of the cell wall, many of which play a determining role in these steps. In addition, C. albicans secretes signaling molecules that inhibit the yeast-to-hypha transition and biofilm formation. In vivo, Candida species are members of mixed biofilms, and subject to various antagonistic and synergistic interactions, which are beginning to be explored. We believe that these new insights will allow for more efficacious treatments of fungal oral infections. For example, the use of signaling molecules that inhibit biofilm formation should be considered. In addition, cell-wall biosynthetic enzymes, wall cross-linking enzymes, and wall proteins, which include adhesins, proteins involved in biofilm formation, fungal-bacterial interactions, and competition for surface colonization sites, offer a wide range of potential targets for therapeutic intervention.

Publisher

SAGE Publications

Subject

General Dentistry

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