ArticleBiology of reproduction2019
Intra-amniotic inflammation induces preterm birth by activating the NLRP3 inflammasome†.
Article in Biology of reproduction, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 111 citations in OpenAlex.
- The amniotic fluid cell-free transcriptome in spontaneous preterm labor.Scientific reports · 2021Trial
- Cellular immune responses in amniotic fluid of women with preterm labor and intra-amniotic infection or intra-amniotic inflammation.American journal of reproductive immunology (New York, N.Y. : 1989) · 2019Trial
- Fetal T Cell Activation in the Amniotic Cavity during Preterm Labor: A Potential Mechanism for a Subset of Idiopathic Preterm Birth.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- Effector and Activated T Cells Induce Preterm Labor and Birth That Is Prevented by Treatment with Progesterone.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- Differential Impact of Bacterial Infection on Preterm Birth in Singleton and Twin Pregnancies and Its Association with Cervical Cerclage or Arabin Pessary: A Retrospective Cohort Study.Journal of clinical medicine · 2026Article
- Mitochondrial dysfunction and cellular senescence drive accelerated gestational aging in spontaneous preterm birth: a narrative review.Apoptosis : an international journal on programmed cell death · 2026Review
- NLRP3 inflammasome characterization in first-trimester, preterm, and term human villous placenta.Scientific reports · 2026Article
- Differential Host Gene Expression Associated with Non-Research square · 2026Article
- Heterogeneity in inflammatory responses to endotoxin at the fetomaternal interface.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Review
- IL-1β stimulates ADAMTS9 expression and contributes to preterm prelabor rupture of membranes.Cell communication and signaling : CCS · 2025Article
- Innate Immune Mechanisms in Normal and Adverse Pregnancy.Advances in experimental medicine and biology · 2025Review
- Review
- Homeostatic Macrophages Prevent Preterm Birth and Improve Neonatal Outcomes by Mitigating In Utero Sterile Inflammation in Mice.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Galectin-1 Elicits a Tissue-Specific Anti-Inflammatory and Anti-Degradative Effect Upon LPS-Induced Response in an Ex Vivo Model of Human Fetal Membranes Modeling an Intraamniotic Inflammation.American journal of reproductive immunology (New York, N.Y. : 1989) · 2024Article
- TLR8-activating miR-146a-3p is an intermediate signal contributing to fetal membrane inflammation in response to bacterial LPS.Immunology · 2024Article
- Article
- Pyroptosis is involved in the immune microenvironment regulation of unexplained recurrent miscarriage.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Article
- Membrane inflammasome activation by choriodecidual Ureaplasma parvum infection without intra-amniotic infection in a Non-Human Primate model†.Biology of reproduction · 2024Article
- Review
20 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Intra-amniotic inflammation is strongly associated with spontaneous preterm labor and birth, the leading cause of perinatal mortality and morbidity worldwide. Previous studies have suggested a role for the NLRP3 (NLR family pyrin domain-containing protein 3) inflammasome in the mechanisms that lead to preterm labor and birth. However, a causal link between the NLRP3 inflammasome and preterm labor/birth induced by intra-amniotic inflammation has not been established. Herein, using an animal model of lipopolysaccharide-induced intra-amniotic inflammation (IAI), we demonstrated that there was priming of the NLRP3 inflammasome (1) at the transcriptional level, indicated by enhanced mRNA expression of inflammasome-related genes (Nlrp3, Casp1, Il1b); and (2) at the protein level, indicated by greater protein concentrations of NLRP3, in both the fetal membranes and decidua basalis prior to preterm birth. Additionally, we showed that there was canonical activation of the NLRP3 inflammasome in the fetal membranes, but not in the decidua basalis, prior to IAI-induced preterm birth as evidenced by increased protein levels of active caspase-1. Protein concentrations of released IL1β were also increased in both the fetal membranes and decidua basalis, as well as in the amniotic fluid, prior to IAI-induced preterm birth. Finally, using the specific NLRP3 inhibitor, MCC950, we showed that in vivo inhibition of the NLRP3 inflammasome reduced IAI-induced preterm birth and neonatal mortality. Collectively, these results provide a causal link between NLRP3 inflammasome activation and spontaneous preterm labor and birth in the context of intra-amniotic inflammation. We also showed that, by targeting the NLRP3 inflammasome, adverse pregnancy and neonatal outcomes can be significantly reduced.
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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.