Identifying Predictors for Inflammation-Induced Preterm Birth: A Murine Study

Authors

Tzu Ning Liu BS, Wayne State University School of Medicine, Department of Obstetrics and GynecologyFollow
Jose Galaz MD, Wayne State University School of Medicine, Department of Obstetrics and Gynecology; Perinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, U.S. Department of Health and Human Services (NICHD/NIH/DHHS)Follow
Nardhy Gomez-Lopez PhD, Wayne State University School of Medicine, Department of Obstetrics and Gynecology; Perinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, U.S. Department of Health and Human Services (NICHD/NIH/DHHS)Follow

Research Mentor Name

Nardhy Gomez-Lopez, PhD

Research Mentor Email Address

ngomezlo@med.wayne.edu

Institution / Department

Wayne State University School of Medicine Department of Obstetrics & Gynecology

Document Type

Research Abstract

Research Type

basicbio

Level of Research

no

Abstract

Introduction: Preterm birth is the leading cause of neonatal morbidity and mortality worldwide. A large proportion of preterm deliveries is affected by intra-amniotic inflammation, which can occur in the presence (intra-amniotic infection) or absence (sterile intra-amniotic inflammation) of microbes. Studies have shown an association between intra-amniotic inflammation, cervical shortening, and changes in the cervicovaginal microbiome. However, their causal relationships are unknown. This study aims to determine the causality of intra-amniotic inflammation, cervical shortening, and cervicovaginal microbiome alterations.

Methods: Pregnant C57BL/6 dams received an ultrasound-guided intra-amniotic injection of an endotoxin lipopolysaccharide (LPS) or the alarmin interleukin-1 alpha (IL-1 alpha) on 16.5 days post-coitum (n = 6-8 per group) to model intra-amniotic infection- or sterile intra-amniotic inflammation-associated preterm birth. Control dams were injected with saline (n=6-8). Cervical length was measured by ultrasound at time zero and 6-hours post-injection. In a second cohort of injected dams, cervical and vaginal tissues were collected 6 hours post-injection (n = 6 per group) for cervicovaginal microbiome analyses via 16S rRNA sequencing.

Results: Dams that received intra-amniotic injections of LPS and IL-1 showed greater percentage of cervical shortening when compared to controls. Microbiome analyses showed taxonomic differences in the bacterial profiles of the cervical and vaginal tissues. However, there were no differences in bacterial profile richness/heterogeneity, composition/structure, and bacterial taxa abundance between the two contrasting groups using generalized linear models, PERMANOVA, LefSe, and ANCOM-BC analyses, respectively.

Conclusion: Alarmin- and endotoxin-induced intra-amniotic inflammation led to cervical shortening, and this was not associated with an acute alteration of the cervicovaginal microbiome.

Disciplines

Female Urogenital Diseases and Pregnancy Complications | Medicine and Health Sciences | Obstetrics and Gynecology | Pathological Conditions, Signs and Symptoms | Reproductive and Urinary Physiology

Recommended Citation

Liu, Tzu Ning BS; Galaz, Jose MD; and Gomez-Lopez, Nardhy PhD, "Identifying Predictors for Inflammation-Induced Preterm Birth: A Murine Study" (2022). Medical Student Research Symposium. 167.
https://digitalcommons.wayne.edu/som_srs/167