ArticleJournal of immunology (Baltimore, Md. : 1950)2020
IRAK1 Is a Critical Mediator of Inflammation-Induced Preterm Birth.
Article in Journal of immunology (Baltimore, Md. : 1950), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The trial behind it
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Evidence for maternal autoantibodies in the pathogenesis of preterm birth.Nature immunology · 2026Article
- miR-146a/b-5p-IRAK1-NF-κB Axis Regulates Unexplained Recurrent Spontaneous Abortion.Journal of molecular recognition : JMR · 2026Article
- Evidence for Maternal Autoantibodies in the Pathogenesis of Preterm Birth.medRxiv : the preprint server for health sciences · 2025Article
- Modulation of the Toll-like Receptor Pathway in Ovine Endometria During Early Pregnancy.Animals : an open access journal from MDPI · 2025Article
- Histological Chorioamnionitis Increases the Risk of Bronchopulmonary Dysplasia.American journal of respiratory and critical care medicine · 2024Article
- Amnion responses to intrauterine inflammation and effects of inhibition of TNF signaling in preterm Rhesus macaque.iScience · 2023Article
- Prematurely delivering mothers show reductions of lachnospiraceae in their gut microbiomes.BMC microbiology · 2023Article
- Genetics, epigenetics, and transcriptomics of preterm birth.American journal of reproductive immunology (New York, N.Y. : 1989) · 2022Review
- Nonhuman Primates in Translational Research.Annual review of animal biosciences · 2022Review
- The landscape of circular RNA in preterm birth.Frontiers in immunology · 2022Article
- Chorioamnionitis and neonatal outcomes.Pediatric research · 2022Review
- The Role of Innate Immune System in the Human Amniotic Membrane and Human Amniotic Fluid in Protection Against Intra-Amniotic Infections and Inflammation.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Preterm birth (PTB) is a major cause of neonatal mortality and morbidity, often triggered by chorioamnionitis or intrauterine inflammation (IUI) with or without infection. Recently, there has been a strong association of IL-1 with PTB. We hypothesized that IL-1R-associated kinase 1 (IRAK1), a key signaling mediator in the TLR/IL-1 pathway, plays a critical role in PTB. In human fetal membranes (FM) collected immediately after birth from women delivering preterm, p-IRAK1 was significantly increased in all the layers of FM with chorioamnionitis, compared with no-chorioamnionitis subjects. In a preterm rhesus macaque model of IUI given intra-amniotic LPS, induction of p-IRAK1 and downstream proinflammatory signaling mediators were seen in the FM. In a C57BL/6J wild-type PTB mouse model of IUI given intrauterine LPS, an IRAK1 inhibitor significantly decreased PTB and increased live birth in a dose-dependent manner. Furthermore, IRAK1 knockout mice were protected from LPS-induced PTB, which was seen in wild-type controls. Activation of IRAK1 was maintained by K63-mediated ubiquitination in preterm FM of humans with chorioamnionitis and rhesus and mouse IUI models. Mechanistically, IRAK1 induced PTB in the mouse model of IUI by upregulating expression of COX-2. Thus, our data from human, rhesus, and mouse demonstrates a critical role IRAK1 in IUI and inflammation-associated PTB and suggest it as potential therapeutic target in IUI-induced PTB.
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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.