ArticleInfection and immunity2010
Epithelial cell-derived S100 calcium-binding proteins as key mediators in the hallmark acute neutrophil response during Candida vaginitis.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 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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Who cites it
87 citing papers in PubMed, 123 citations in OpenAlex.
- Saccharomyces cerevisiae reduces vulvovaginal candidiasis severity through modulation of fungal pathogenicity and inflammatory responses.Nature communications · 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
- 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
- Candida albicans migrates itself from the vagina to the uterus and ovaries in estrogenized mice.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2025Article
- Vaginal Candida albicans infections: host-pathogen-microbiome interactions.FEMS microbiology reviews · 2025Review
- Transcriptomic insights into early responses of the uterovaginal junction and vagina to avian influenza virus infection in turkey breeder hens.Frontiers in physiology · 2025Article
- 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
- Anti-Microorganisms · 2023Article
- Defensins: defenders of human reproductive health.Human reproduction update · 2023Review
- The Role of Host and Fungal Factors in the Commensal-to-Pathogen Transition ofCurrent clinical microbiology reports · 2023Review
- A New Approach for the Treatment of Recurrent Vulvovaginal Candidiasis with a Combination of Pea Protein, Grape Seed Extract, and Lactic Acid Assessed In Vivo.Journal of fungi (Basel, Switzerland) · 2022Article
- The antimicrobial activity of zinc against group B Streptococcus is strain-dependent across diverse sequence types, capsular serotypes, and invasive versus colonizing isolates.BMC microbiology · 2022Article
- Antiviral lectin Q-Griffithsin suppresses fungal infection in murine models of vaginal candidiasis.Frontiers in cellular and infection microbiology · 2022Article
- Methods Related to the Immunopathogenesis of Vulvovaginal Candidiasis and Associated Neutrophil Anergy.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Association between Human Genetic Variants and the Vaginal Bacteriome of Pregnant Women.mSystems · 2021Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Vulvovaginal candidiasis (VVC), caused by Candida species, is a significant problem in women of childbearing age. Similar to clinical observations, a robust vaginal polymorphonuclear neutrophil (PMN) migration occurs in a subset of mice without affecting vaginal fungal burden. We hypothesize that the vaginal PMN infiltrate and accompanying inflammation are not protective but instead are responsible for the symptoms of infection. The purpose of this study was to identify the signal(s) associated with the PMN response in the established mouse model. Vaginal lavage fluid from inoculated mice were categorized base on PMN counts, evaluated for PMN chemotactic activity and analyzed by SDS-PAGE and mass spectrometry (MS) for unique protein identification. The lavage fluid from inoculated mice with high, but not low, PMN levels showed increased chemotactic activity. Likewise, SDS-PAGE of lavage fluid with high PMN levels showed distinct protein patterns. MS revealed that bands at 6 and 14 kDa matched the PMN chemotactic calcium-binding proteins (CBPs), S100A8 and S100A9, respectively. The presence of the CBPs in lavage fluid was confirmed by Western blots and enzyme-linked immunosorbent assay. Vaginal tissues and epithelial cells from inoculated mice with high PMN levels stained more intensely and exhibited increased mRNA transcripts for both proteins compared to those in mice with low PMN levels. Subsequent antibody neutralization showed significant abrogation of the chemotactic activity when the lavage fluid was treated with anti-S100A8, but not anti-S100A9, antibodies. These results reveal that the PMN chemotactic CBP S100A8 and S100A9 are produced by vaginal epithelial cells following interaction with Candida and that S100A8 is a strong candidate responsible for the robust PMN migration during experimental VVC.
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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 Socratic graph.