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The commensal fungus,  Candida albicans , can cause life-threatening infections in at risk individuals.  C .  albicans  colonizes mucosal surfaces of most people, adhering to and interacting with epithelial cells. At low concentrations,  C .  albicans  is not pathogenic nor does it cause epithelial cell damage  in vitro ; at high concentrations,  C .  albicans  causes mucosal infections and kills epithelial cells  in vitro . Here we show that while there are quantitative dose-dependent differences in exposed epithelial cell populations, these reflect a fundamental qualitative difference in host cell response to  C .  albicans . Using transcriptional profiling experiments and real time PCR, we found that wild-type  C .  albicans  induce dose-dependent responses from a FaDu epithelial cell line. However, real time PCR and Western blot analysis using a high dose of various  C .  albicans  strains demonstrated that these dose-dependent responses are associated with ability to promote host cell damage. Our studies support the idea that epithelial cells play a key role in the immune system by monitoring the microbial community at mucosal surfaces and initiating defensive responses when this community is dysfunctional. This places epithelial cells at a pivotal position in the interaction with  C .  albicans  as epithelial cells themselves promote  C .  albicans  stimulated damage.

Human Epithelial Cells Discriminate between Commensal and Pathogenic Interactions with Candida albicans