S ALTMEIER¹, F SCHÖNHERR¹, S AMORIM-VAZ², VDU T TRAN³, AT COSTE², D SANGLARD², S LEIBUNDGUT-LANDMANN<sup>1

1</sup>Section of Immunology, Vetsuisse Faculty, University of Zürich, Winterthurerstrasse 266a, 8057 Zurich, Switzerland, ²Institute of Microbiology, University of Lausanne and University Hospital Center, Rue du Bugnon 48, 1011 Lausanne, Switzerland, ³Swiss Institute of Bioinformatics, University of Lausanne, CIG - Quartier Sorge, Bâtiment Génopode, 1015 Lausanne, Switzerland

Candida albicans is one of the most important disease-causing fungi in humans. Infections of the oral and vaginal mucosa are by far the most frequent disease manifestations affecting millions of people worldwide. While C. albicans lives as a commensal on mucosal surfaces of most healthy individuals, it can become pathogenic under certain circumstances. Predisposing conditions include immunosuppression and acquired or congenital immunodeficiencies. Disease development may also be influenced by the variation in fungal virulence that exists among C. albicans strains in the population. Here, we used a genome-wide transcriptomic approach in combination with a mouse model of oropharyngeal candidiasis to study the mutual response of the fungus and the host within the infected tissue. The host expression profiles reveal a dynamic regulation of the host response pathways and uncover novel candidate genes involved in the response to C. albicans. Applying this approach to mice infected with different fungal isolates of high and low pathogenicity revealed major differences in the transcriptional response to these isolates that reflect their disparate capacity to persist in the host mucosa. Together, these data advance our current understanding of the interaction between C. albicans isolates and the mucosal epithelium, which is of paramount importance for understanding the factors that determine the fine balance between commensalism and infection.