Mutual adaptation of C. albicans and the host in the stably colonized murine tongue tissue

The human commensal fungus C. albicans colonizes the oral mucosa of most healthy individuals. Homeostasis at the fungus-host interface depends strictly on the IL-17 pathway. To understand the mutual adaptations of C. albicans and the host in the oral mucosa and to assess the IL-17-dependence thereof, we employed a mouse model of long-term C. albicans colonization and transcriptionally profiled the colonized tongue tissue at day 3 and day 19. The antifungal response is strongly induced on day 3 after colonization, with many antimicrobial factors being induced in an IL-17-dependent manner. Due to fungal overgrowth and exacerbated tissue invasion in IL-17-deficient mice, the transcriptome is dominated by a plethora of inflammatory genes such as Il-20 family, Il-17a/f, Il-13 and IFNy, by day 19. Only few fungal transcripts could be reliably be detected, given that the fungal transcripts represent only a small proportion of the entire RNA and without enrichment. They support the notion that C. albicans adopts virulence features in the IL-17-deficient host einvironment with increased expression of hyphae specific genes like HWP1. Gene expression profiling (RNA-seq) of C.albicans strain 101 grown in YPD broth, and of murine tongues of Il-17rc-/- or Il-17rc+/- mice that were associated with C. albicans strain 101 for 3 days or 19 days. The samples with low candida concentrations that we sequenced deep to get sufficient candida reads. The raw file linked to the '*_B' sample was used to generate the candida prcessed data file, and the raw file linked to the corresponding *_A sample was used to generate the mouse processed file.