ArticleThe Journal of infectious diseases2019
Candidalysin Is Required for Neutrophil Recruitment and Virulence During Systemic Candida albicans Infection.
Article in The Journal of infectious diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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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
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Who cites it
75 citing papers in PubMed, 102 citations in OpenAlex.
- Delineating the Concerted Action of Virulence Attributes in Candida albicans Systemic Infection.Journal of cellular and molecular medicine · 2026Article
- The transcription factor Ahr1 governs the recruitment of neutrophils to the brain and clearance ofmBio · 2026Article
- From Oral Candidiasis to Candidemia: A Review of Superficial to Invasive Progression.MicrobiologyOpen · 2026Review
- Article
- Dangerous liaisons: Candidalysin and myeloid cells in candidiasis.PLoS pathogens · 2026Article
- Fungi and colorectal cancer: from dysregulation to clinical translation.Gut pathogens · 2026Review
- MUC16-dependent Renal Vascular Adhesion of Candida Promotes Tissue Invasion and Predicts Clinical Outcome in Candidemia.Research square · 2026Article
- Fungal infection drives metabolic reprogramming in epithelial cells via aerobic glycolysis and an alternative TCA cycle shunt.Science advances · 2026Article
- Candidalysin at the epithelial-systemic interface: mechanistic evidence, critical-care relevance, and translational opportunities in invasive candidiasis.Frontiers in cellular and infection microbiology · 2026Review
- The pathogenicity and future treatment strategies ofFrontiers in cellular and infection microbiology · 2026Review
- Microbiota-based therapies in oral health and disorders.Folia microbiologica · 2025Review
- Detection of serum anti-candidalysin IgG by indirect ELISA: a novel auxiliary tool for diagnosing invasive candidiasis in a preliminary pediatric study.Microbiology spectrum · 2025Article
- Anti-Inflammatory Potential of Extracellular Polysaccharide from the Moss EndophyteMicroorganisms · 2025Article
- Insights into the evolution of Candidalysin and recent developments.Archives of microbiology · 2025Review
- Review
- Host targets of candidalysin.PLoS pathogens · 2025Review
- Essential role of hepcidin in host resistance to disseminated candidiasis.Cell reports · 2025Article
- Review
- Vaginal Candida albicans infections: host-pathogen-microbiome interactions.FEMS microbiology reviews · 2025Review
- Advancements in vaginal microbiota,Microbial cell (Graz, Austria) · 2025Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 9 institutions in 4 countries.
Funding
Abstract
backgroundCandidalysin is a cytolytic peptide toxin secreted by Candida albicans hyphae and has significantly advanced our understanding of fungal pathogenesis. Candidalysin is critical for mucosal C albicans infections and is known to activate epithelial cells to induce downstream innate immune responses that are associated with protection or immunopathology during oral or vaginal infections. Furthermore, candidalysin activates the NLRP3 inflammasome and causes cytolysis in mononuclear phagocytes. However, the role of candidalysin in driving systemic infections is unknown.
methodsIn this study, using candidalysin-producing and candidalysin-deficient C albicans strains, we show that candidalysin activates mitogen-activated protein kinase (MAPK) signaling and chemokine secretion in endothelial cells in vitro.
resultsCandidalysin induces immune activation and neutrophil recruitment in vivo, and it promotes mortality in zebrafish and murine models of systemic fungal infection.
conclusionsThe data demonstrate a key role for candidalysin in neutrophil recruitment and fungal virulence during disseminated systemic C albicans infections.
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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.