Exacerbation of Candida Albicans Pathogenicity by Oral Bacteria

Objectives: Candida albicans is an opportunistic pathogen and key commensal which forms interkingdom relationships with several different bacterial species in the oral cavity. These interactions are thought to influence the progression of disease and how the host responds in inflammatory oral diseases such as periodontitis and denture stomatitis. The purpose of this study is to investigate the interactions at a transcriptional and functional level between Candida albicans and different commensal and pathogenic oral bacterial species such as Streptococcus gordonii, Porphyromonas gingivalis and Fusobacterium nucleatum. Method: Dual-species and multi-species biofilm models were created by introducing oral bacterial species to pre-existing C. albicans biofilms. Microbiological quantification for all biofilms were determined using colony forming units (CFUs). Transcriptional responses were assessed using transcriptomic analysis. Functional assays were used to investigate key gene pathways upregulated in multi-species biofilm models: of note, evaluate of the hemin uptake and its effect on C. albicans growth were assessed using spectroscopic profiling. Results: Our work demonstrated using CFU counts that C. albicans was essential to support the growth of P. gingivalis and F. nucleatum in oxygenated environment. The transcriptional analysis of C. albicans biofilm revealed an increase in gene transcripts which encode for iron uptake in the presence of the three oral bacterial biofilms. Our results showed that the Csa2 hemin-uptake protein in C. albicans has affinity for the hemin that utilized by P. gingivalis, and the hemin could play a crucial role in regulating filamentation in C. albicans. Conclusion: Our findings provide an insight into the interaction between C. albicans and oral microbial species, and the role of these microorganisms in aggravating C. albicans pathogenicity. This highlights important consideration of C. albicans has a key pathogen in oral dysbiosis when co-colonised alongside important bacterial colonisers of health vs disease.