| Literature DB >> 27923704 |
Heather R Conti1, Vincent M Bruno2, Erin E Childs3, Sean Daugherty2, Joseph P Hunter4, Bemnet G Mengesha4, Danielle L Saevig4, Matthew R Hendricks3, Bianca M Coleman3, Lucas Brane3, Norma Solis5, J Agustin Cruz3, Akash H Verma3, Abhishek V Garg3, Amy G Hise6, Jonathan P Richardson7, Julian R Naglik7, Scott G Filler5, Jay K Kolls8, Satrajit Sinha9, Sarah L Gaffen10.
Abstract
Signaling through the IL-17 receptor (IL-17R) is required to prevent oropharyngeal candidiasis (OPC) in mice and humans. However, the IL-17-responsive cell type(s) that mediate protection are unknown. Using radiation chimeras, we were able to rule out a requirement for IL-17RA in the hematopoietic compartment. We saw remarkable concordance of IL-17-controlled gene expression in C. albicans-infected human oral epithelial cells (OECs) and in tongue tissue from mice with OPC. To interrogate the role of the IL-17R in OECs, we generated mice with conditional deletion of IL-17RA in superficial oral and esophageal epithelial cells (Il17raΔK13). Following oral Candida infection, Il17raΔK13 mice exhibited fungal loads and weight loss indistinguishable from Il17ra-/- mice. Susceptibility in Il17raΔK13 mice correlated with expression of the antimicrobial peptide β-defensin 3 (BD3, Defb3). Consistently, Defb3-/- mice were susceptible to OPC. Thus, OECs dominantly control IL-17R-dependent responses to OPC through regulation of BD3 expression.Entities:
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Year: 2016 PMID： 27923704 PMCID： PMC5147498 DOI： 10.1016/j.chom.2016.10.001
Source DB: PubMed Journal: Cell Host Microbe ISSN： 1931-3128 Impact factor: 21.023