ArticleAmerican journal of reproductive immunology (New York, N.Y. : 1989)2019
The tracking of lipopolysaccharide through the feto-maternal compartment and the involvement of maternal TLR4 in inflammation-induced fetal brain injury.
Article in American journal of reproductive immunology (New York, N.Y. : 1989), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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Who cites it
29 citing papers in PubMed, 36 citations in OpenAlex.
- Trophoblast stem cells and syncytiotrophoblasts lack inflammatory responses to LPS but retain robust interferon-mediated antiviral immunity.Reproduction & fertility · 2026Article
- Synbiotic Nutraceutical Mitigates Gestational Diabetes Effects and Cardiovascular Dysfunction in Rat Offspring.Molecular nutrition & food research · 2026Article
- Heat stress-induced gut dysbiosis and multi-organ injury: mechanisms and therapeutic modulation.Frontiers in cellular and infection microbiology · 2026Review
- Maternal consumption of urbanized diet compromises early-life health in association with gut microbiota.Gut microbes · 2025Review
- Hypoxia Supports LPS-Driven Tolerance and Functional Activation in BV-2 Microglial Cells.Biology · 2025Article
- Inverted day-night feeding during pregnancy affects the brain health of both maternal and fetal brains through increasing inflammation levels associated with dysbiosis of the gut microbiome in rats.Journal of neuroinflammation · 2025Article
- Ascending Vaginal Infection in Mice Induces Preterm Birth and Neonatal Morbidity.The American journal of pathology · 2025Article
- Fatty acid composition in the vaginal tract of cis-gender women: canary in coal mines for reproductive health?Lipids in health and disease · 2025Review
- The Importance of Including Maternal Immune Activation in Animal Models of Hypoxic-Ischemic Encephalopathy.Biomedicines · 2024Article
- C/EBPδ deficiency delays infection-induced preterm birth.BMC medicine · 2024Article
- Maternal obesity alters fetal neuroinflammation in a murine model of preterm birth.AJOG global reports · 2024Article
- Dysbiotic Vaginal Microbiota Induces Preterm Birth Cascade via Pathogenic Molecules in the Vagina.Metabolites · 2024Article
- Deciphering maternal-fetal cross-talk in the human placenta during parturition using single-cell RNA sequencing.Science translational medicine · 2024Article
- Decreased level of TREM like Transcript 1 (TLT-1) is associated with prematurity and promotes the in-utero inflammatory response to maternal lipopolysaccharide (LPS) exposure.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- A key role for NLRP3 signaling in preterm labor and birth driven by the alarmin S100B.Translational research : the journal of laboratory and clinical medicine · 2023Article
- The fetal response to maternal inflammation is dependent upon maternal IL-6 in a murine model.Cytokine · 2023Article
- Regulatory mechanisms of HMGB1 and its receptors in polycystic ovary syndrome-driven gravid uterine inflammation.The FEBS journal · 2023Article
- FGL2 deficiency alleviates maternal inflammation-induced blood-brain barrier damage by blocking PI3K/NF-κB mediated endothelial oxidative stress.Frontiers in immunology · 2023Article
- Article
- Differential Brain and Cerebrospinal Fluid Proteomic Responses to Acute Prenatal Endotoxin Exposure.Molecular neurobiology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
problemExposure to intrauterine inflammation (IUI) has been shown to induce fetal brain injury and increase the risk of acquiring a neurobehavioral disorder. The trafficking of the inflammatory mediator, lipopolysaccharide (LPS), in the pregnant female reproductive tract in the setting of IUI and the precise mechanisms by which inflammation induces fetal brain injury are not fully understood. METHOD OF STUDY: FITC-labeled LPS was utilized to induce IUI on E15, tissues were collected, and fluorescence was visualized via the Spectrum IVIS. Embryo transfer was utilized to create divergent maternal and fetal genotypes. Wild-type (WT) embryos were transferred into TLR4-/- pseudopregnant dams (TLR4-/-
resultsLipopolysaccharide trafficked to the uterus, fetal membranes, placenta, and the fetus and was undetectable in other tissues. Endotoxin was present in the amniotic fluid of all animals exposed to LPS. However, the immune response was blunted in TLR4-/-
conclusionIntrauterine administered LPS is capable of accessing the entire feto-placental unit with or without a functional maternal TLR4. Thus, bacteria or bacterial byproducts in the uterus may negatively impact fetal development regardless of the maternal genotype or endotoxin response. Despite the blunted immune response in the TLR4-deficient dams, an inflammatory response is still ignited in the amniotic cavity and may negatively impact the fetus.
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