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CME Credit Offered
CME Credit Offered
Abstract Award
Abstract Award
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Poster Session 3

(810) Vaginal polyamines modify Gardnerella vaginalis-induced alterations in the mucosal transcriptome

Friday, January 31, 2025
10:30 AM – 12:30 PM  

    Presenting Author(s)

  • Lauren Anton, PhD (she/her/hers)

    Research Assistant Professor
    University of Pennsylvania Perelman School of Medicine
    Philadelphia, PA, United States

    • Coauthor(s)

  • BF

    Briana Ferguson, BA (she/her/hers)

    University of Pennsylvania Perelman School of Medicine
    Smyrna, Delaware, United States

  • AL

    Aaron Loder, BA

    University of Pennsylvania Perelman School of Medicine
    Philadelphia, Pennsylvania, United States

    • Submitting Author(s)

  • Kristin D. Gerson, MD, PhD

    Assistant Professor of Obstetrics and Gynecology Assistant Professor of Microbiology
    University of Pennsylvania Perelman School of Medicine
    Philadelphia, PA, United States

Objective:

Anaerobe-dominant cervicovaginal (CV) microbial communities increase risk of preterm birth. Mucus production, a key part of the host defense system, protects the CV epithelial barrier against anaerobes, including Gardnerella vaginalis(GV). Vaginal anaerobes modify mucus properties though molecular mechanisms remain unclear. We previously showed that vaginal metabolites, specifically polyamines, regulate GV-induced host immune responses. This study aimed to 1) elucidate effects of GV on genes involved in mucus biosynthesis, and 2) determine whether polyamines modify GV-altered mucosal gene expression.


Study Design:

Human ectocervical (Ecto), endocervical (Endo) and vaginal (VK2) epithelial cells were treated for 4h +/- polyamines, spermine (SPM, 400uM) or putrescine (PUT, 4mM) prior to GV (107 CFU/well) exposure for 24h (n=3/treatment). RNA-sequencing was performed. Data were analyzed using DESeq2 to study mucus genes of interest. For genes altered by GV, analysis of polyamine exposure was performed by one-way ANOVA with Tukey’s test for multiple comparisons.


Results:

Among the 40 mucus-associated genes studied, GV modified expression of 10 genes in Ectos, 13 genes in Endos, and 6 genes in VK2s (p< 0.05 for all). Genes clustered into functional pathways including mucins, ion channels, protein disulfide isomerases, glycosyl-transferases, and mucus modifying enzymes (select pathways shown for Ecto in Fig. 1 and Endo in Fig 2.). Among genes altered by GV, SPM partially mitigated these effects in select cells for TMEM38A, SLC12A6, PDIA3, PDIA4, PDIA6, GALNT5, SLPI and NEU1, while PUT potentiated these effects in select cells for TMEM38A, SLC12A6, SLC26A9, PACC1, SLPI, NEU1 (p< 0.05 for all).


Conclusion:

GV modifies expression of genes in the CV epithelium responsible for increased mucus hydration, formation, and breakdown (sialidases). These alterations in the mucosal transcriptome likely compromise mucus properties, rendering mucus thinner and more penetrable. SPM confers protection against some of these GV-induced effects and may carry potential as a postbiotic therapeutic to restore mucus function.