Human Epithelial Cells Discriminate between Commensal and Pathogenic Interactions with Candida albicans
AffiliationUniv Arizona, Dept Ecol & Evolutionary Biol
MetadataShow full item record
PublisherPublic Library of Science
CitationHuman Epithelial Cells Discriminate between Commensal and Pathogenic Interactions with Candida albicans 2016, 11 (4):e0153165 PLOS ONE
Rights© 2016 Rast et al. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
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AbstractThe 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.
VersionFinal published version
SponsorsFunded by University of Minnesota (http://www.research.umn.edu): #18805, National Institutes of Health (http://www.niaid.nih.gov/Pages/default.aspx): 1R01 AI064054-01, and Burroughs Wellcome Fund (http://www.bwfund.org): #1004419. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.