ArticleBiology of reproduction2014
Human fetal membranes generate distinct cytokine profiles in response to bacterial Toll-like receptor and nod-like receptor agonists.
Article in Biology of reproduction, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 88 citations in OpenAlex.
- The Role of Complement and CD4 T Cells in Preeclampsia and Offspring Neurodevelopment.Current opinion in physiology · 2026Article
- Towards microbiome-informed strategies for predicting and preventing pregnancy complications.Reproduction & fertility · 2026Review
- Neutrophil extracellular traps in pregnancy complications.Frontiers in immunology · 2026Review
- Article
- Intermediate Signaling Mechanisms Regulating Human Fetal Membrane Responses to Gram-Positive Bacterial Peptidoglycan.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Article
- Buprenorphine induces human fetal membrane sterile inflammation.Journal of reproductive immunology · 2025Article
- Maternal Psychotherapy Addressing Generational Stress is Associated with Lower Preterm Birth Risk: The Pforzheim Study.Women's health reports (New Rochelle, N.Y.) · 2025Article
- Contractile responses of engineered humanAPL bioengineering · 2024Article
- TLR8-activating miR-146a-3p is an intermediate signal contributing to fetal membrane inflammation in response to bacterial LPS.Immunology · 2024Article
- Maternal Infection and Preterm Birth: From Molecular Basis to Clinical Implications.Children (Basel, Switzerland) · 2023Review
- Intrinsic sexual dimorphism in the placenta determines the differential response to benzene exposure.iScience · 2023Article
- The serotonin reuptake inhibitor fluoxetine induces human fetal membrane sterile inflammation through p38 MAPK activation.Journal of reproductive immunology · 2023Article
- Mechanisms of immune regulation by the placenta: Role of type I interferon and interferon-stimulated genes signaling during pregnancy.Immunological reviews · 2022Review
- Human fetal membrane IL-1β production in response to bacterial components is mediated by uric-acid induced NLRP3 inflammasome activation.Journal of reproductive immunology · 2022Article
- Impact of Progesterone on Molecular Mechanisms of Preterm Premature Rupture of Membranes.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Polymicrobial stimulation of human fetal membranes induce neutrophil activation and neutrophil extracellular trap release.Journal of reproductive immunology · 2021Article
- Activated Neutrophils Propagate Fetal Membrane Inflammation and Weakening through ERK and Neutrophil Extracellular Trap-Induced TLR-9 Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Novel pathways of inflammation in human fetal membranes associated with preterm birth and preterm pre-labor rupture of the membranes.Seminars in immunopathology · 2020Review
- Viral infection dampens human fetal membrane type I interferon responses triggered by bacterial LPS.Journal of reproductive immunology · 2020Article
- Foetal lung volumes in pregnant women who deliver very preterm: a pilot study.Pediatric research · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Bacterial infection-associated inflammation is thought to be a major cause of preterm premature rupture of membranes. Proinflammatory cytokines, such as interleukin 1B (IL1B), can weaken fetal membranes (FM) by upregulating matrix metalloproteinases and inducing apoptosis. The mechanism by which infection leads to inflammation at the maternal-fetal interface and subsequent preterm birth is thought to involve innate immune pattern recognition receptors (PRR), such as the Toll-like receptors (TLR) and Nod-like receptors (NLR), which recognize pathogen-associated molecular patterns (PAMPs). The objective of this study was to determine the cytokine profile generated by FMs in response to the bacterial TLR and NLR agonists peptidoglycan (PDG; TLR2), lipopolysaccharide (LPS; TLR4), flagellin (TLR5), CpG ODN (TLR9), iE-DAP (Nod1), and MDP (Nod2). PDG, LPS, flagellin, iE-DAP, and MDP triggered FMs to generate an inflammatory response, but the cytokine profiles were distinct for each TLR and NLR agonist, and only IL1B and RANTES were commonly upregulated in response to all five PAMPs. CpG ODN, in contrast, had a mild stimulatory effect only on MCP-1 and primarily downregulated basal FM cytokine production. IL1B secretion induced by PDG, LPS, flagellin, iE-DAP, and MDP was associated with its processing. Furthermore, FM IL1B secretion in response to TLR2, TLR4, and TLR5 activation was caspase 1-dependent, whereas Nod1 and Nod2 induced IL1B secretion independent of caspase 1. These findings demonstrate that FMs respond to different bacterial TLR and NLR PAMPs by generating distinct inflammatory cytokine profiles through distinct mechanisms that are specific to the innate immune PRR activated.
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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.