ArticlePLoS pathogens2024
Candida albicans translocation through the intestinal epithelial barrier is promoted by fungal zinc acquisition and limited by NFκB-mediated barrier protection.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 28 citations in OpenAlex.
- COVID-19-Associated Fungal Co-Infections: Pathogenesis, Diagnostics, Biomarkers, and Therapeutic Strategies.Journal of clinical medicine · 2026Review
- Cytokine signalling in vaginal epithelial cells: mechanistic insights into epithelial immunity and inflammatory milieu in vulvovaginal candidiasis.European cytokine network · 2026Review
- Cross-kingdom microbial interactions in the gut during inflammatory bowel disease.Journal of translational medicine · 2026Review
- Fungal Reactive Oxygen Species Secreted byJournal of fungi (Basel, Switzerland) · 2026Article
- The role of the gut mycobiota in neurodevelopmental disorders: a multikingdom disruption of the gut-brain axis.Frontiers in microbiology · 2026Review
- Engineering Organoid Platforms for Pathogenesis Research.Research (Washington, D.C.) · 2026Review
- Oral microbiome contribution in colorectal carcinogenesis: polymicrobial interactions and virulence determinants.Frontiers in cellular and infection microbiology · 2026Review
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- From intestinal immune niches to systemic inflammation: programming cellular plasticity and immune redistribution across organs.Frontiers in immunology · 2026Review
- Targeting the gut microbiome for type 2 diabetes management: a scoping review of systematic reviews and meta-analyses.Frontiers in endocrinology · 2026Article
- Article
- The fungal peptide toxin candidalysin induces distinct membrane repair mechanisms compared to bacterial pore-forming toxins.Cell death discovery · 2025Article
- Enhancement of melanoma aggressiveness via p38-MAPK, HIF-1α pathways, and metabolic reprogramming induced by Candida albicans.Scientific reports · 2025Article
- Relationship Between Virulence Factor Activities, Cytotoxicity ofDentistry journal · 2025Article
- Dynamic expression of candidalysin facilitates oral colonization of Candida albicans in mice.Nature microbiology · 2025Article
- "Pour some sugar on me"-Environmental Candida albicans isolates and the evolution of increased pathogenicity and antifungal resistance through sugar adaptation.PLoS pathogens · 2025Article
- Article
- Commensal colonization ofMicrobiology spectrum · 2025Article
- Commensalism and pathogenesis of Candida albicans at the mucosal interface.Nature reviews. Microbiology · 2025Review
- Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
The opportunistic fungal pathogen Candida albicans thrives on human mucosal surfaces as a harmless commensal, but frequently causes infections under certain predisposing conditions. Translocation across the intestinal barrier into the bloodstream by intestine-colonizing C. albicans cells serves as the main source of disseminated candidiasis. However, the host and microbial mechanisms behind this process remain unclear. In this study we identified fungal and host factors specifically involved in infection of intestinal epithelial cells (IECs) using dual-RNA sequencing. Our data suggest that host-cell damage mediated by the peptide toxin candidalysin-encoding gene ECE1 facilitates fungal zinc acquisition. This in turn is crucial for the full virulence potential of C. albicans during infection. IECs in turn exhibit a filamentation- and damage-specific response to C. albicans infection, including NFκB, MAPK, and TNF signaling. NFκB activation by IECs limits candidalysin-mediated host-cell damage and mediates maintenance of the intestinal barrier and cell-cell junctions to further restrict fungal translocation. This is the first study to show that candidalysin-mediated damage is necessary for C. albicans nutrient acquisition during infection and to explain how IECs counteract damage and limit fungal translocation via NFκB-mediated maintenance of the intestinal barrier.
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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.