Basic Science
Poster Session 2
Briana Ferguson, BA, MS
University of Pennsylvania, Perelman School of Medicine
Philadelphia, PA, United States
Dylan Curry, BS
University of Pennsylvania, Perelman School of Medicine
Philadelphia, PA, United States
Elliot Friedman, PhD
University of Pennsylvania, Perelman School of Medicine
Philadelphia, PA, United States
Jennifer A. McCoy, MD, MSCE (she/her/hers)
Assistant Professor
University of Pennsylvania Perelman School of Medicine
Philadelphia, PA, United States
Paul J. Planet, MD, PhD
Children's Hospital of Philadelphia
Philadelphia, PA, United States
Dustin Flannery, DO, MSCE
Children's Hospital of Philadelphia
Philadelphia, PA, United States
Karen Puopolo, MD, PhD
Children's Hospital of Philadelphia
Philadelphia, PA, United States
Lauren Anton, PhD
University of Pennsylvania, Perelman School of Medicine
Philadelphia, PA, United States
Kristin D. Gerson, MD, PhD
Assistant Professor of Obstetrics and Gynecology
Assistant Professor of Microbiology
Hospital of the University of Pennsylvania
Philadelphia, PA, United States
Group B Streptococcus (GBS) disease, the leading cause of early-onset neonatal sepsis, is predicated upon vaginal colonization. Given limitations of existing screening and prophylaxis strategies, primary prevention of GBS disease necessitates interventions targeting vaginal colonization. Features of vaginal ecosystems may modify GBS colonization though mechanisms are incompletely understood. We sought to investigate how common vaginal microbes modify GBS growth at epithelial barriers.
Study Design:
Ectocervical, endocervical, and vaginal (VK2) epithelial cells were treated with Gardnerella vaginalis (G. vaginalis) or Lactobacillus crispatus (L. crispatus) for 24h. Cell culture (conditioned) media was sterile filtered. Clinical isolates of GBS serotypes Ia, III, and IV were grown in varying concentrations (50%, 75%, 100%) of conditioned media. Optical density was measured across time points to create GBS growth curves. Growth at 8h was compared across groups by one-way ANOVA with Dunnett’s tests for multiple comparisons. Fold change comparing GBS growth in G. vaginalis-conditioned epithelial cell media to L. crispatus-conditioned epithelial cell media was calculated to generate heat maps.
Results:
GBS growth was higher in media from G. vaginalis-conditioned epithelia compared to L. crispatus-conditioned epithelia for all GBS serotypes (Fig. 1, p < 0.05 for all). Effects of conditioned media from ectocervical, endocervical, and vaginal epithelial cells on GBS growth were similar. GBS serotypes responded similarly to conditioned media.
Conclusion:
Exposure of the cervicovaginal epithelium to G. vaginalis, an anaerobe implicated in adverse reproductive outcomes, promotes growth of clinical GBS isolates involved in invasive disease. L. crispatus exerts a relative protective effect. Microbial-conditioning of the cervicovaginal epithelium likely plays a mechanistic role in the complex microbial ecology governing GBS colonization – interventions aimed at optimizing host responses to components of vaginal ecosystems may offer novel approaches to GBS eradication in pregnancy.