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Group B streptococcus activates transcriptomic pathways related to premature birth in human extraplacental membranes
Hae-Ryung Park1,2, Sean M Harris1, Erica Boldenow1,3
1Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA.
Insights
Group B Streptococcus (GBS) infection in pregnant women triggers inflammation and preterm birth pathways in extraplacental membranes within hours. This study reveals early molecular targets of GBS, offering insights into adverse pregnancy outcomes.
Area of Science:
- Obstetrics and Gynecology
- Infectious Diseases
- Molecular Biology
Background:
- Group B Streptococcus (GBS) is a leading cause of neonatal infectious morbidity and mortality.
- The link between GBS infection and preterm birth is not fully understood.
- Early molecular mechanisms of GBS interaction with gestational tissues are poorly defined.
Purpose of the Study:
- To investigate the hypothesis that short-term GBS inoculation activates inflammation and preterm birth pathways in human extraplacental membranes.
- To identify early molecular events following GBS interaction with gestational tissues.
- To elucidate the contribution of GBS to adverse pregnancy outcomes.
Main Methods:
- In vitro inoculation of human extraplacental membranes with GBS.
- Microarray-based transcriptomics to analyze gene expression changes.
- Measurement of prostaglandin E2 (PGE2), matrix metalloproteinases 1 (MMP1), and 3 (MMP3) levels.
Main Results:
- GBS inoculation rapidly activated pathways related to inflammation and preterm birth, with significant changes observed as early as 4 hours post-inoculation.
- Gene expression pathways involved in DNA replication and repair were downregulated following GBS treatment.
- Elevated levels of PGE2, MMP1, and MMP3 were observed, consistent with roles in parturition and premature rupture of membranes.
Conclusions:
- Short-term GBS exposure initiates molecular pathways associated with inflammation and preterm birth in human extraplacental membranes.
- GBS infection impacts key cellular processes including DNA replication and repair.
- The findings provide novel molecular targets for understanding and potentially preventing GBS-associated adverse pregnancy outcomes.
Abstract:
Streptococcus agalactiae (group B streptococcus [GBS]) infection in pregnant women is the leading cause of infectious neonatal morbidity and mortality in the United States. Although inflammation during infection has been associated with preterm birth, the contribution of GBS to preterm birth is less certain. Moreover, the early mechanisms by which GBS interacts with the gestational tissue to affect adverse pregnancy outcomes are poorly understood. We hypothesized that short-term GBS inoculation activates pathways related to inflammation and premature birth in human extraplacental membranes. We tested this hypothesis using GBS-inoculated human extraplacental membranes in vitro. In agreement with our hypothesis, a microarray-based transcriptomics analysis of gene expression changes in GBS-inoculated membranes revealed that GBS activated pathways related to inflammation and preterm birth with significant gene expression changes occurring as early as 4 h postinoculation. In addition, pathways related to DNA replication and repair were downregulated with GBS treatment. Conclusions based on our transcriptomics data were further supported by responses of prostaglandin E2 (PGE2), and matrix metalloproteinases 1 (MMP1) and 3 (MMP3), all of which are known to be involved in parturition and premature rupture of membranes. These results support our initial hypothesis and provide new information on molecular targets of GBS infection in human extraplacental membranes.
