ArticlePLoS pathogens2016
The Extracellular Matrix of Candida albicans Biofilms Impairs Formation of Neutrophil Extracellular Traps.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
What it found
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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.
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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.
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Who cites it
88 citing papers in PubMed, 129 citations in OpenAlex.
- Persistent NET states link lesion-related microbial signals to the cold tumor-related local restrictive environment: a context-dependent working model.Cell communication and signaling : CCS · 2026Review
- Saccharomyces cerevisiae reduces vulvovaginal candidiasis severity through modulation of fungal pathogenicity and inflammatory responses.Nature communications · 2026Article
- Candida in the lung: Fact, fiction, friend or foe?PLoS pathogens · 2026Article
- Natural-Compound Adjuvants Dismantle Candida Biofilms: Mechanisms, Design Rules, and Biofilm-Aware Pharmacology.Current microbiology · 2026Review
- Vitamin C enhances corneal fungal infection treatment in mice via chemotaxis and anti-inflammation.Antimicrobial agents and chemotherapy · 2026Article
- The IL-17A/TNFSF10 axis promotes vulvovaginal candidiasis pathogenesis by inducing neutrophil necroptosis.Frontiers in cellular and infection microbiology · 2026Article
- Review
- Review
- Vaginal mycobiome characteristics and therapeutic strategies in vulvovaginal candidiasis (VVC): differentiating pathogenic species and microecological features for stratified treatment.Clinical microbiology reviews · 2025Review
- Bloodstream infections: mechanisms of pathogenesis and opportunities for intervention.Nature reviews. Microbiology · 2025Review
- Biofilm-Associated Candidiasis: Pathogenesis, Prevalence, Challenges and Therapeutic Options.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Candida albicans aspartyl protease (Sap6) inhibits neutrophil function via a "Trojan horse" mechanism.Scientific reports · 2025Article
- Neutrophils: emerging perspectives on the pathogenesis of oral mucosal diseases.Frontiers in cellular and infection microbiology · 2025Review
- Molecular mechanisms of neutrophil regulatory network in anti-Candida infection.Frontiers in immunology · 2025Review
- The hypoxic microenvironment ofFrontiers in immunology · 2025Article
- Host immune response against fungal biofilms.Current opinion in microbiology · 2024Review
- Fungal vaccines and adjuvants: a tool to reveal the interaction between host and fungi.Archives of microbiology · 2024Review
- Impaired neutrophil extracellular trap-forming capacity contributes to susceptibility to chronic vaginitis in a mouse model of vulvovaginal candidiasis.Infection and immunity · 2024Article
- Understanding Type 3 Innate Lymphoid Cells and Crosstalk with the Microbiota: A Skin Connection.International journal of molecular sciences · 2024Review
- Complexation of fungal extracellular nucleic acids by host LL-37 peptide shapes neutrophil response toFrontiers in immunology · 2024Article
28 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
8 authors at 1 institution in 1 country.
Funding
Abstract
Neutrophils release extracellular traps (NETs) in response to planktonic C. albicans. These complexes composed of DNA, histones, and proteins inhibit Candida growth and dissemination. Considering the resilience of Candida biofilms to host defenses, we examined the neutrophil response to C. albicans during biofilm growth. In contrast to planktonic C. albicans, biofilms triggered negligible release of NETs. Time lapse imaging confirmed the impairment in NET release and revealed neutrophils adhering to hyphae and migrating on the biofilm. NET inhibition depended on an intact extracellular biofilm matrix as physical or genetic disruption of this component resulted in NET release. Biofilm inhibition of NETosis could not be overcome by protein kinase C activation via phorbol myristate acetate (PMA) and was associated with suppression of neutrophil reactive oxygen species (ROS) production. The degree of impaired NET release correlated with resistance to neutrophil attack. The clinical relevance of the role for extracellular matrix in diminishing NET production was corroborated in vivo using a rat catheter model. The C. albicans pmr1Δ/Δ, defective in production of matrix mannan, appeared to elicit a greater abundance of NETs by scanning electron microscopy imaging, which correlated with a decreased fungal burden. Together, these findings show that C. albicans biofilms impair neutrophil response through an inhibitory pathway induced by the extracellular matrix.
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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.