ArticleJournal of clinical immunology2022
Candidalysin, a Virulence Factor of Candida albicans, Stimulates Mast Cells by Mediating Cross-Talk Between Signaling Pathways Activated by the Dectin-1 Receptor and MAPKs.
Article in Journal of clinical immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- Gut-Brain Inflammation and Disrupted Homeostasis Due to Activation of Mast Cells and Microglia.International journal of molecular sciences · 2026Review
- Discovery of the High-Affinity Aptamer for Candidalysin Using a Dual-Mode Colorimetric-SERS Platform.Biosensors · 2026Article
- Innate airway immune response to fungal allergens.Frontiers in immunology · 2026Review
- Tight junction suppression by candidalysin promotes gut-to-blood dissemination ofFrontiers in microbiology · 2026Article
- Molecular mechanisms, pathogenesis and therapeutic advances ofFrontiers in cellular and infection microbiology · 2026Review
- Eosinophil CD48 interactions with Candida albicans Als6 is protective in vitro and in mouse systemic candidiasis.Nature communications · 2025Article
- Aberrant Activation of Mast Cells: Molecular Mechanisms and Targets for Intervention.Clinical reviews in allergy & immunology · 2025Review
- Enhanced virulence of mixed-species Candida biofilms isolated from intragastric balloon patient: insights from larval model.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2025Article
- Fungi and cancer: unveiling the complex role of fungal infections in tumor biology and therapeutic resistance.Frontiers in cellular and infection microbiology · 2025Review
- Article
- Fungal feelings in the irritable bowel syndrome: the intestinal mycobiome and abdominal pain.Gut microbesReview
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
purposeAlthough mast cells (MCs) modulate the activity of effector cells during Candida albicans infection, their role in the pathogenesis of candidiasis remains unclear. Candidalysin, a C. albicans-derived peptide toxin, is a crucial factor in fungal infections. We aimed to investigate the effect of candidalysin on MC activation and the underlying molecular mechanism.
methodsSerum from candidalysin-immunized mice was used to measure candidalysin expression in patients infected with C. albicans. MC degranulation and migration were evaluated by β-hexosaminidase release assay and chemotaxis assay, respectively. EIA and ELISA were used to evaluate the production of eicosanoids and cytokines/chemokines, respectively. The production of nitric oxide (NO) was measured with a DAF-FM diacetate kit, while reactive oxygen species (ROS) production was analyzed by flow cytometry. MAPK activation was evaluated by Western blotting.
resultsWe detected high candidalysin expression in the lesions of patients infected with C. albicans, and the MC number was increased in these lesions. LL-37 colocalized with MCs in the lesions of candidiasis patients. Candidalysin-enhanced MC accumulation in mice and treating LAD2 and HMC-1 cells with candidalysin induced their degranulation, migration, and production of pro- and anti-inflammatory cytokines/chemokines, eicosanoids, ROS, NO, and LL-37. Interestingly, C. albicans strains lacking candidalysin failed to induce MC activation. Moreover, candidalysin increased dectin-1 expression, and the inhibition of dectin-1 decreased MC activation. Downstream dectin-1 signaling involved the MAPK pathways.
conclusionThe finding that candidalysin causes cutaneous MC activation may improve our understanding of the role of MCs in the pathology of cutaneous C. albicans infection.
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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.