Candida glabrata and Candida albicans co-infection of an in vitro oral epithelium
Candida albicans is regarded as the leading of candidosis. However, Candida glabrata has emerged as an important pathogen of oral mucosa, occurring both singly or in mixed species infections, often with C. albicans. Compared with C. albicans, little is known about the role of C. glabrata in oral infection. The aim of this study was to examine single and mixed species infection of oral epithelium involving C. glabrata and establish its ability to invade and damage tissue. Methods:
A reconstituted human oral epithelium (RHOE) was infected only with C. glabrata, or simultaneously with C. glabrata and C. albicans. The ability of both species to invade the tissue was examined using species specific peptide nucleic acid (PNA) probe hybridization and confocal laser scanning microscopy. Epithelial damage was assessed by measuring lactate dehydrogenase (LDH) activity. Results:
Candida glabrata strains were able to colonize the RHOE, in a strain dependent manner. Candida glabrata single infection after 12 h, generally revealed no invasion of the RHOE, which contrasted with extensive tissue invasion demonstrated by C. albicans. Mixed infection showed that C. albicans enhanced the invasiveness of C. glabrata, and led to increased LDH release by the RHOE, which paralleled the observed histological damage. Conclusions:
The results obtained demonstrating enhanced invasion and increased tissue damage caused by mixed C. glabrata and C. albicans infections have important clinical significance and highlight the need to identify Candida species involved in oral candidosis.
Document Type: Research Article
Affiliations: 1: Institute for Biotechnology and Bioengineering, Universidade do Minho, Campus de Gualtar 4710-057, Braga, Portugal 2: School of Biosciences, Cardiff University, Park Place, Cardiff, CF10 3US, UK 3: Tissue Engineering and Reparative Dentistry, School of Dentistry, Cardiff University, Heath Park, Cardiff, CF14 4XY, UK
Publication date: 01 May 2011