| Summary: | As more information emerges on oral microbiota using advanced sequencing methodologies, it is imperative to examine how organisms modulate the capacity of each other to colonize or trigger infection. Most mouse models of oral <i>C. albicans</i> infection have focused on interactions with single bacterial species. Thus, little is known about the microbiome-mediated interactions that control the switch of <i>C. albicans</i> from commensalism to infection. Evidence is accumulating that in immunosuppression where mucosal candidiasis is more prevalent, there is an altered oral bacterial microbiome with reduced diversity, but not an altered mycobiome. Oropharyngeal candidiasis in immunosuppressed humans and mice is associated with a further reduction in oral bacterial diversity and a dysbiotic shift with significant enrichment of streptococcal and enterococcal species. Our recent studies in a cancer chemotherapy mouse model supported the combined profound effect of immunosuppression and <i>C. albicans</i> in reducing oral bacterial diversity and provided the first direct evidence that these changes contribute to pathogenesis, representing dysbiosis. There is still a gap in understanding the relationship between <i>Candida</i> and the oral bacterial microbiome. We propose that certain oral commensal bacteria contribute to fungal pathogenesis and we identify gaps in our understanding of the mechanisms involved in this cooperative virulence.
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