Poster Session 3
Category: Prematurity
Poster Session 3
Gregory W. Kirschen, MD, PhD (he/him/his)
MFM Fellow
University of Pennsylvania Perelman School of Medicine
Philadelphia, Pennsylvania, United States
Kristin M. Klohonatz, PhD
University of Pennsylvania Perelman School of Medicine
Philadelphia, Pennsylvania, United States
Lauren Anton, PhD (she/her/hers)
Research Assistant Professor
University of Pennsylvania Perelman School of Medicine
Philadelphia, Pennsylvania, United States
Kristin D. Gerson, MD, PhD
Assistant Professor of Obstetrics and Gynecology
Assistant Professor of Microbiology
University of Pennsylvania
Hospital of the university of Pennsylvania, Pennsylvania, United States
Gardnerella vaginalis (GV) colonization of the cervicovaginal (CV) space is associated with adverse perinatal outcomes including preterm birth (PTB). Mechanisms by which GV drives outcomes remain largely unknown. Oxidative stress promotes physiologic cervical ripening in term parturition. We hypothesized that GV induces oxidative imbalance in the CV epithelial barrier as a potential mechanism underlying premature cervical remodeling preceding PTB.
We co-cultured GV or Lactobacillus crispatus (LC), a healthy vaginal microbe, at 105-107 CFU/well with ectocervical (Ecto), endocervical (Endo), and vaginal (VK2) epithelial cells for 24h. We assessed two markers of oxidative stress: 1) thiobarbituric acid reactive substances (TBARS), a byproduct of lipid peroxidation, was measured in cell culture media; and 2) activity of superoxide dismutase (SOD), a key antioxidant enzyme, was measured in cell lysate. Data were analyzed by one-way ANOVA with Tukey’s test for multiple comparisons.
GV induced TBARS for Ecto, Endo, and VK2 cells in a dose-dependent manner across all cell lines compared to non-treated (NT) and microbial control LC (p< 0.05 for all, Fig. 1). GV similarly induced SOD activity in a dose-dependent manner across all cell lines compared to NT and LC controls (p< 0.05 for all, Fig. 2).
A vaginal anaerobe implicated in the pathophysiology of PTB induces oxidative stress in the CV epithelium. These molecular events likely contribute to the molecular pathophysiology of premature cervical remodeling. Antioxidant-based therapeutics may serve as a novel strategy to reduce PTB among individuals with microbiota-related risk. 1R01HD114611-01 (KDG)