IADR Abstract Archives
Contact-dependent inhibition of Candida albicans hyphal morphogenesis by Fusobacterium nucleatum
Objectives: Candida albicans and Fusobacterium nucleatum are two well-known pathogens involved in various oral diseases. Previously, we demonstrated that F. nucleatum ATCC 23726 coaggregates with C. albicans SN152, a process mediated by RadD and FLO9, two membrane proteins from F. nucleatum and C. albicans, respectively. This study was aimed at investigating whether these two microorganisms interact each other beyond physical attachment.
Methods: Yeast or hyphal forms of C. albicans SN152 wildtype and FLO9 mutant were co-cultivated with F. nucleatum ATCC 23726 wildtype or radD mutant, and the inhibition of C. albicans hyphal morphogenesis was monitored and visualized by light microscopy. A two-chamber assay in which the cells were physically separated by a 0.4-μm PET membrane insert while sharing the same growth medium was used to determine if the inhibition of hyphal morphogenesis was contact-dependent. An in vitro killing assay was performed in which co-culture of F. nucleatum with yeast or hyphal form of C. albicans was incubated with RAW macrophages, and the surviving C. albicans were determined by colony counting.
Results: We showed that F. nucleatum ATCC 23726 inhibits hyphal morphogenesis of C. albicans SN152 in a contact-dependent manner. Further analysis revealed that the observed contact-depended inhibition of Candida hyphal morphogenesis is mediated via the C. albicans membrane protein FLO9 and F. nucleatum RadD, the protein pair that mediates physical attachment between these two microorganisms. Furthermore, the killing assay showed that compared to the hyphal form, the F. nucleatum-induced yeast form of C. albicans was more resistant to killing by RAW cells.
Conclusions: Our study suggested that C. albicans might trade virulence (hyphae) for long-term fitness by maintaining the yeast form through physical interaction with F. nucleatum. This finding could impact our understanding of inter-kingdom signaling communications and affect clinical treatment strategy.
Methods: Yeast or hyphal forms of C. albicans SN152 wildtype and FLO9 mutant were co-cultivated with F. nucleatum ATCC 23726 wildtype or radD mutant, and the inhibition of C. albicans hyphal morphogenesis was monitored and visualized by light microscopy. A two-chamber assay in which the cells were physically separated by a 0.4-μm PET membrane insert while sharing the same growth medium was used to determine if the inhibition of hyphal morphogenesis was contact-dependent. An in vitro killing assay was performed in which co-culture of F. nucleatum with yeast or hyphal form of C. albicans was incubated with RAW macrophages, and the surviving C. albicans were determined by colony counting.
Results: We showed that F. nucleatum ATCC 23726 inhibits hyphal morphogenesis of C. albicans SN152 in a contact-dependent manner. Further analysis revealed that the observed contact-depended inhibition of Candida hyphal morphogenesis is mediated via the C. albicans membrane protein FLO9 and F. nucleatum RadD, the protein pair that mediates physical attachment between these two microorganisms. Furthermore, the killing assay showed that compared to the hyphal form, the F. nucleatum-induced yeast form of C. albicans was more resistant to killing by RAW cells.
Conclusions: Our study suggested that C. albicans might trade virulence (hyphae) for long-term fitness by maintaining the yeast form through physical interaction with F. nucleatum. This finding could impact our understanding of inter-kingdom signaling communications and affect clinical treatment strategy.