Candida albicans is the most abundant and frequently isolated commensal fungal species in healthy adults. However, it is also an opportunistic pathogen that can cause localized or systemic infections under certain circumstances – most notably when there is a disruption to the bacterial microbiota. Our lab demonstrated that C. albicans plays a disproportionate role in modulating the reassembly of lactic acid bacteria (LAB) communities in mice following broad-spectrum antibiotic treatment. Specifically, colonization with C. albicans led to diminished levels of Lactobacillus johnsonii and outgrowth of Enterococcus faecalis, which share physical and metabolic niches with C. albicans along the gastrointestinal (GI) tract. This suggests that the interactions between C. albicans and LAB are critical for regulating C. albicans colonization and persistence, which are prerequisites for pathogenesis. Moreover, L. johnsonii and E. faecalis have been shown to modulate C. albicans growth and morphogenesis, indicating that these interactions are bidirectional. Despite this striking observation, the mechanisms underlying their interplay have not been investigated. To address this gap, we are implementing global transcriptomics as a screening tool to identify differentially expressed genes in C. albicans in the presence of L. johnsonii and/or E. faecalis. We plan to use a microaerobic co-culture setup, which will better reflect the oxygen gradient in mucosal layers of the GI tract where these organisms reside. Our findings from these experiments will provide important insight into the mechanisms of interaction between C. albicans, L. johnsonii, and E. faecalis, and the role of these interactions in C. albicans persistence in the GI tract.
