Protection against epithelial damage during Candida albicans infection is mediated by PI3K/Akt and mammalian target of rapamycin signaling.
J Infect Dis
; 209(11): 1816-26, 2014 Jun 01.
Article
em En
| MEDLINE
| ID: mdl-24357630
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.
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Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Candida albicans
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Fosfatidilinositol 3-Quinases
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Células Epiteliais
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Proteínas Proto-Oncogênicas c-akt
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Serina-Treonina Quinases TOR
Limite:
Humans
Idioma:
En
Ano de publicação:
2014
Tipo de documento:
Article