Candida glabrata Binding to Candida albicans Hyphae Enables Its Development in Oropharyngeal Candidiasis

Abstract

Pathogenic mechanisms of Candida glabrata in oral candidiasis, especially because of its inability to form hyphae, are understudied. Since both Candida albicans and C. glabrata are frequently co-isolated in oropharyngeal candidiasis (OPC), we examined their co-adhesion in vitro and observed adhesion of C. glabrata only to C. albicans hyphae microscopically. Mice were infected sublingually with C. albicans or C. glabrata individually, or with both species concurrently, to study their ability to cause OPC. Infection with C. glabrata alone resulted in negligible infection of tongues; however, colonization by C. glabrata was increased by co-infection or a pre-established infection with C. albicans. Furthermore, C. glabrata required C. albicans for colonization of tongues, since decreasing C. albicans burden with fluconazole also reduced C. glabrata. C. albicans hyphal wall adhesins Als1 and Als3 were important for in vitro adhesion of C. glabrata and to establish OPC. C. glabrata cell wall protein coding genes EPA8, EPA19, AWP2, AWP7, and CAGL0F00181 were implicated in mediating adhesion to C. albicans hyphae and remarkably, their expression was induced by incubation with germinated C. albicans. Thus, we found a near essential requirement for the presence of C. albicans for both initial colonization and establishment of OPC infection by C. glabrata.

Study of Microbial Interaction Formed by "Candida krusei" and "Candida glabrata": "In Vitro" and "In Vivo" Studies

“…Based on the CFU/mL data analysis of yeast recovered from the buccal cavity of immunosuppressed mice with single infections, the recovery observed were equivalent to 6.05 log10 for groups infected with C. krusei and 4.49 log10 for groups infected with C. glabrata, showing that C. krusei had a higher colonization ability compared to C. glabrata. The low CFU count of C. glabrata is consistent with Tati et al (25) who tried to establish a model of oropharyngeal candidiasis with C. glabrata. The authors used inocula size of ranging 1x10 10 cells/mL and recovered 4-7x10 2 cells/mL from the tongue.…”

Candida albicans–epithelial interactions and induction of mucosal innate immunity

“…Mice lacking these defensins show markedly increased susceptibility to OPC [30,69•,71]. IL-17 may also act on salivary gland cells, contributing to the production of antifungal AMPs such as histatins [72,73]. The combined action of IL-17 signaling promotes effective, non-redundant host defense to mucosal candidiasis.…”

The vaginal mycobiome: A contemporary perspective on fungi in women's health and diseases

“…While pathogenic mechanisms attributed to single fungal species have consumed much of mycology, it is believed that mycobiome studies will establish correlation between composition and function of the entire fungal community, and cross-kingdom interactions to disease processes. Notably, fungi-fungi interactions have been implicated in the pathogenic process; C. glabrata binds to the hyphae of C. albicans to establish oropharyngeal candidiasis, 129 thus supporting the need for mycobiome studies that consider the full context in which infection takes place. Culture-based isolation and characterization of pathogens remains of great necessity, however, development of novel in vitro (and even in vivo) models of polymicrobial communities would be ideal to test hypotheses into the role of the vaginal mycobiome in health and disease.…”