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J Infect Dis. 2014 Jun 1;209(11):1816-26. doi: 10.1093/infdis/jit824. Epub 2013 Dec 19.

Protection against epithelial damage during Candida albicans infection is mediated by PI3K/Akt and mammalian target of rapamycin signaling.

Author information

1
Department of Oral Immunology, King's College London Dental Institute.

Abstract

BACKGROUND:

The ability of epithelial cells (ECs) to discriminate between commensal and pathogenic microbes is essential for healthy living. Key to these interactions are mucosal epithelial responses to pathogen-induced damage.

METHODS:

Using reconstituted oral epithelium, we assessed epithelial gene transcriptional responses to Candida albicans infection by microarray. Signal pathway activation was monitored by Western blotting and transcription factor enzyme-linked immunosorbent assay, and the role of these pathways in C. albicans-induced damage protection was determined using chemical inhibitors.

RESULTS:

Transcript profiling demonstrated early upregulation of epithelial genes involved in immune responses. Many of these genes constituted components of signaling pathways, but only NF-κB, MAPK, and PI3K/Akt pathways were functionally activated. We demonstrate that PI3K/Akt signaling is independent of NF-κB and MAPK signaling and plays a key role in epithelial immune activation and damage protection via mammalian target of rapamycin (mTOR) activation.

CONCLUSIONS:

PI3K/Akt/mTOR signaling may play a critical role in protecting epithelial cells from damage during mucosal fungal infections independent of NF-κB or MAPK signaling.

KEYWORDS:

Akt; Candida albicans; MAPK; PI3 kinase; c-Fos; damage; epithelial; fungal; inflammation; mTOR; microarray

PMID:
24357630
PMCID:
PMC4017362
DOI:
10.1093/infdis/jit824
[Indexed for MEDLINE]
Free PMC Article

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