ArticleBiology of reproduction2018
Group B streptococcus activates transcriptomic pathways related to premature birth in human extraplacental membranes in vitro.
Article in Biology of reproduction, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Group B streptococcus induces cellular senescence in human amnion epithelial cells through a partial interleukin-1-mediated mechanism.Biology of reproduction · 2024Article
- The antioxidant N-acetyl cysteine inhibits cytokine and prostaglandin release in human fetal membranes stimulated ex vivo with lipoteichoic acid or live group B streptococcus.American journal of reproductive immunology (New York, N.Y. : 1989) · 2024Article
- Maternal Group B Streptococcus Infection Correlates Inversely With Preeclampsia in Pregnant African American Women.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2024Article
- Emerging role of toll-like receptors signaling and its regulators in preterm birth: a narrative review.Archives of gynecology and obstetrics · 2023Review
- Characterisation of the consequences of maternal immune activation on distinct cell populations in the developing rat spinal cord.Journal of anatomy · 2022Article
- Sepsis in a Seropositive Pregnant Woman With Early Preterm Labor Pains: A Case Study of a Near Miss.Cureus · 2022Article
- Molecular mechanisms of environmental toxin cadmium at the feto-maternal interface investigated using an organ-on-chip (FMi-OOC) model.Journal of hazardous materials · 2022Article
- Streptococcus pyogenes infects human endometrium by limiting the innate immune response.The Journal of clinical investigation · 2021Article
- Toxicant Disruption of Immune Defenses: Potential Implications for Fetal Membranes and Pregnancy.Frontiers in physiology · 2020Article
- Modulation of Death and Inflammatory Signaling in Decidual Stromal Cells following Exposure to Group BInfection and immunity · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.