ArticleThe Journal of infectious diseases2014
Protection against epithelial damage during Candida albicans infection is mediated by PI3K/Akt and mammalian target of rapamycin signaling.
Article in The Journal of infectious diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 103 citations in OpenAlex.
- Article
- Saccharomyces cerevisiae reduces vulvovaginal candidiasis severity through modulation of fungal pathogenicity and inflammatory responses.Nature communications · 2026Article
- Enhancement of melanoma aggressiveness via p38-MAPK, HIF-1α pathways, and metabolic reprogramming induced by Candida albicans.Scientific reports · 2025Article
- Commensalism and pathogenesis of Candida albicans at the mucosal interface.Nature reviews. Microbiology · 2025Review
- Article
- Exploring the therapeutic mechanism of itraconazole combined with ritonavir onFrontiers in pharmacology · 2025Article
- 3D human epithelial models: a promising platform for studyingFrontiers in cellular and infection microbiology · 2025Article
- EGR1 regulates oral epithelial cell responses toVirulence · 2024Article
- Candida albicans translocation through the intestinal epithelial barrier is promoted by fungal zinc acquisition and limited by NFκB-mediated barrier protection.PLoS pathogens · 2024Article
- Specific cell subclusters of dental pulp stem cells respond to distinct pathogens through the ROS pathway.Frontiers in cellular and infection microbiology · 2024Article
- New anticancer therapeutics impact fungal pathobiology, infection dynamics, and outcome.PLoS pathogens · 2023Article
- Candida albicans induces neutrophil extracellular traps and leucotoxic hypercitrullination via candidalysin.EMBO reports · 2023Article
- IκBζ is an essential mediator of immunity to oropharyngeal candidiasis.Cell host & microbe · 2023Article
- Host's Immunity andMicroorganisms · 2022Review
- TheScience signaling · 2022Article
- "Molding" immunity-modulation of mucosal and systemic immunity by the intestinal mycobiome in health and disease.Mucosal immunology · 2022Review
- The IL-20RB receptor and the IL-20 signaling pathway in regulating host defense in oral mucosal candidiasis.Frontiers in cellular and infection microbiology · 2022Article
- Fungi-A Component of the Oral Microbiome Involved in Periodontal Diseases.Advances in experimental medicine and biology · 2022Article
- Article
- Candidalysin triggers epithelial cellular stresses that induce necrotic death.Cellular microbiology · 2021Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe 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.
methodsUsing 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.
resultsTranscript 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.
conclusionsPI3K/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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.