ArticleNature communications2019
Candidalysin activates innate epithelial immune responses via epidermal growth factor receptor.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
126 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.
- Pooled it
- Microbe-Derived Antimicrobial Peptides: Immunomodulation and Gut Microbiota Homeostasis.Microorganisms · 2026Review
- Review
- Dangerous liaisons: Candidalysin and myeloid cells in candidiasis.PLoS pathogens · 2026Article
- Cytokine signalling in vaginal epithelial cells: mechanistic insights into epithelial immunity and inflammatory milieu in vulvovaginal candidiasis.European cytokine network · 2026Review
- Cervicovaginal Mycobiome Restructuring by HPV and Bacterial Community State Types in a Kazakhstani Shotgun Metagenomic Cohort:International journal of molecular sciences · 2026Article
- An IL-17-DUOX2 axis controls gastrointestinal colonization by Candida albicans.Nature communications · 2026Article
- Glycogen phosphorylase L confers metabolic flexibility in neutrophils to fight fungal infections in nutrient-deprived tissues.Cell host & microbe · 2026Article
- Article
- Fungal infection drives metabolic reprogramming in epithelial cells via aerobic glycolysis and an alternative TCA cycle shunt.Science advances · 2026Article
- Article
- Candidalysin at the epithelial-systemic interface: mechanistic evidence, critical-care relevance, and translational opportunities in invasive candidiasis.Frontiers in cellular and infection microbiology · 2026Review
- Pulmonary injury in inflammatory bowel disease: intestinal barrier disruption, gut-lung axis remodeling, and treatment-related lung toxicity.Frontiers in immunology · 2026Review
- Aerolysin-like proteins fromFrontiers in fungal biology · 2026Article
- The pathogenicity and future treatment strategies ofFrontiers in cellular and infection microbiology · 2026Review
- The fungal peptide toxin candidalysin induces distinct membrane repair mechanisms compared to bacterial pore-forming toxins.Cell death discovery · 2025Article
- A Pseudomonas aeruginosa quorum-sensing inducer controls lung permeability in establishing chronic infection via EGFR.Nature communications · 2025Article
- PMA1-containing extracellular vesicles ofGut microbes · 2025Article
- Candida albicans Enhances Protease Activity and Activates MyD88-Dependent IL-1β Production in Human Keratinocytes.Mycoses · 2025Article
- The multi-kingdom cancer microbiome.Nature microbiology · 2025Review
66 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 6 institutions in 4 countries.
Funding
Abstract
Candida albicans is a fungal pathobiont, able to cause epithelial cell damage and immune activation. These functions have been attributed to its secreted toxin, candidalysin, though the molecular mechanisms are poorly understood. Here, we identify epidermal growth factor receptor (EGFR) as a critical component of candidalysin-triggered immune responses. We find that both C. albicans and candidalysin activate human epithelial EGFR receptors and candidalysin-deficient fungal mutants poorly induce EGFR phosphorylation during murine oropharyngeal candidiasis. Furthermore, inhibition of EGFR impairs candidalysin-triggered MAPK signalling and release of neutrophil activating chemokines in vitro, and diminishes neutrophil recruitment, causing significant mortality in an EGFR-inhibited zebrafish swimbladder model of infection. Investigation into the mechanism of EGFR activation revealed the requirement of matrix metalloproteinases (MMPs), EGFR ligands and calcium. We thus identify a PAMP-independent mechanism of immune stimulation and highlight candidalysin and EGFR signalling components as potential targets for prophylactic and therapeutic intervention of mucosal candidiasis.
Indexed as
Identifiers
What OpenQuestion holds
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.