ArticleInfection and immunity2014
Vaginal epithelial cell-derived S100 alarmins induced by Candida albicans via pattern recognition receptor interactions are sufficient but not necessary for the acute neutrophil response during experimental vaginal candidiasis.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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.
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Who cites it
51 citing papers in PubMed, 67 citations in OpenAlex.
- Epitope unmasking in vulvovaginal candidiasis is associated with hyphal growth and neutrophilic infiltration.PloS one · 2018Trial
- Cytokine signalling in vaginal epithelial cells: mechanistic insights into epithelial immunity and inflammatory milieu in vulvovaginal candidiasis.European cytokine network · 2026Review
- An In Vitro A-431 Epithelial Cell Infection Model for Studying Fungal Pathogenicity and Immune Responses Associated With Vulvovaginal Candidiasis.Bio-protocol · 2026Article
- State-of-the-Art Review: Managing Vulvovaginal Candidiasis.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2026Review
- Biphasic Regulation of Epithelial Antimicrobial Peptides DuringJournal of fungi (Basel, Switzerland) · 2026Article
- Elevated vaginal heparan sulfate correlates with impaired neutrophil killing ofInfection and immunity · 2026Article
- Cervicovaginal microbiome alters transcriptomic and chromatin accessibility signatures across cervicovaginal epithelial barriers.Microbiome · 2025Article
- Article
- Exploring the vaginal ecosystem: insights into host-microbe interactions and microbial community dynamics.Infection and immunity · 2025Review
- Use of Intravaginal Cooling to Provide Symptom Relief in Women With Vulvovaginal Candidiasis and Reduce Immunopathology in an Accompanying Mouse Model.The Journal of infectious diseases · 2025Article
- New insights toward personalized therapies for vulvovaginal candidiasis and vaginal co-infections.Frontiers in microbiology · 2025Review
- Host-microbe interaction paradigms in acute and recurrent vulvovaginal candidiasis.Cell host & microbe · 2024Review
- Transcriptomics Reveals Effect ofPharmaceuticals (Basel, Switzerland) · 2024Article
- Impaired neutrophil extracellular trap-forming capacity contributes to susceptibility to chronic vaginitis in a mouse model of vulvovaginal candidiasis.Infection and immunity · 2024Article
- Inflammatory cytokine signalling in vulvovaginal candidiasis: a hot mess driving immunopathology.Oxford open immunology · 2024Review
- The Interplay betweenMicroorganisms · 2023Review
- Methods Related to the Immunopathogenesis of Vulvovaginal Candidiasis and Associated Neutrophil Anergy.Methods in molecular biology (Clifton, N.J.) · 2022Article
- The impact of the Fungus-Host-Microbiota interplay upon Candida albicans infections: current knowledge and new perspectives.FEMS microbiology reviews · 2021Review
- Immune Sensing ofJournal of fungi (Basel, Switzerland) · 2021Review
- It Takes Two to Tango: How a Dysregulation of the Innate Immunity, Coupled WithFrontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Vulvovaginal candidiasis (VVC), caused by Candida albicans, affects women worldwide. Animal and clinical studies suggest that the immunopathogenic inflammatory condition of VVC is initiated by S100 alarmins in response to C. albicans, which stimulate polymorphonuclear neutrophil (PMN) migration to the vagina. The purpose of this study was to extend previous in vitro data and determine the requirement for the alarmin S100A8 in the PMN response and to evaluate pattern recognition receptors (PRRs) that initiate the response. For the former, PMN migration was evaluated in vitro or in vivo in the presence or absence of S100 alarmins initiated by several approaches. For the latter, vaginal epithelial cells were evaluated for PRR expression and C. albicans-induced S100A8 and S100A9 mRNAs, followed by evaluation of the PMN response in inoculated PRR-deficient mice. Results revealed that, consistent with previously reported in vitro data, eukaryote-derived S100A8, but not prokaryote-derived recombinant S100A8, induced significant PMN chemotaxis in vivo. Conversely, a lack of biologically active S100A8 alarmin, achieved by antibody neutralization or by using S100A9(-/-) mice, had no effect on the PMN response in vivo. In PRR analyses, whereas Toll-like receptor 4 (TLR4)- and SIGNR1-deficient vaginal epithelial cells showed a dramatic reduction in C. albicans-induced S100A8/S100A9 mRNAs in vitro, inoculated mice deficient in these PRRs showed PMN migration similar to that in wild-type controls. These results suggest that S100A8 alarmin is sufficient, but not necessary, to induce PMN migration during VVC and that the vaginal PMN response to C. albicans involves PRRs in addition to SIGNR1 and TLR4, or other induction pathways.
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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.