ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Regulation of apoptosis and innate immune stimuli in inflammation-induced preterm labor.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- Human labour is associated with altered regulatory T cell function and maternal immune activation.Clinical and experimental immunology · 2020Trial
- Effector and Activated T Cells Induce Preterm Labor and Birth That Is Prevented by Treatment with Progesterone.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- Inflammation at the maternal-fetal interface: a perspective on interacting risk factors for preterm birth in sub-Saharan African women living with HIV.Frontiers in immunology · 2026Review
- Caspase-3, Caspase-8 and XIAP Gene Expression in the Placenta: Exploring the Causes of Spontaneous Preterm Labour.International journal of molecular sciences · 2023Article
- Myometrial-derived CXCL12 promotes lipopolysaccharide induced preterm labour by regulating macrophage migration, polarization and function in mice.Journal of cellular and molecular medicine · 2022Article
- IL-22 Plays a Dual Role in the Amniotic Cavity: Tissue Injury and Host Defense against Microbes in Preterm Labor.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Review
- HSP70: an alarmin that does not induce high rates of preterm birth but does cause adverse neonatal outcomes.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2021Article
- Clostridioides difficile Toxin A Remodels Membranes and Mediates DNA Entry Into Cells to Activate Toll-Like Receptor 9 Signaling.Gastroenterology · 2020Article
- Novel pathways of inflammation in human fetal membranes associated with preterm birth and preterm pre-labor rupture of the membranes.Seminars in immunopathology · 2020Review
- Cell-Free Fetal DNA Increases Prior to Labor at Term and in a Subset of Preterm Births.Reproductive sciences (Thousand Oaks, Calif.) · 2020Article
- Tendril extract ofInternational journal of medical sciences · 2020Article
- The Role of Danger Associated Molecular Patterns in Human Fetal Membrane Weakening.Frontiers in physiology · 2020Review
- Immunobiology of Acute Chorioamnionitis.Frontiers in immunology · 2020Review
- Gasdermin D: Evidence of pyroptosis in spontaneous preterm labor with sterile intra-amniotic inflammation or intra-amniotic infection.American journal of reproductive immunology (New York, N.Y. : 1989) · 2019Article
- Inflammasomes: Their Role in Normal and Complicated Pregnancies.Journal of immunology (Baltimore, Md. : 1950) · 2019Review
- Elevated maternal retinoic acid-related orphan receptor-γt enhances the effect of polyinosinic-polycytidylic acid in inducing fetal loss.Experimental animals · 2019Article
- Sepsis: Precision-Based Medicine for Pregnancy and the Puerperium.International journal of molecular sciences · 2019Review
- Article
- Are B cells altered in the decidua of women with preterm or term labor?American journal of reproductive immunology (New York, N.Y. : 1989) · 2019Article
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Authors and funding
6 authors.
Funding
Abstract
An innate immune response is required for successful implantation and placentation. This is regulated, in part, by the a2 isoform of V-ATPase (a2V) and the concurrent infiltration of M1 (inflammatory) and M2 (anti-inflammatory) macrophages to the uterus and placenta. The objective of the present study was to identify the role of a2V during inflammation-induced preterm labor in mice and its relationship to the regulation of apoptosis and innate immune responses. Using a mouse model of infection-induced preterm delivery, gestational tissues were collected 8 h after intrauterine inoculation on day 14.5 of pregnancy with either saline or peptidoglycan (PGN; a TLR 2 agonist) and polyinosinic-polycytidylic acid [poly(I:C); a TLR3 agonist], modeling Gram-positive bacterial and viral infections, respectively. Expression of a2V decreased significantly in the placenta, uterus, and fetal membranes during PGN+poly(I:C)-induced preterm labor. Expression of inducible NO synthase was significantly upregulated in PGN+poly(I:C)-treated placenta and uterus. PGN+poly(I:C) treatment disturbed adherens junction proteins and increased apoptotic cell death via an extrinsic pathway of apoptosis among uterine decidual cells and spongiotrophoblasts. F4/80(+) macrophages were increased and polarization was skewed in PGN+poly(I:C)-treated uterus toward double-positive CD11c(+) (M1) and CD206(+) (M2) cells, which are critical for the clearance of dying cells and rapid resolution of inflammation. Expression of Nlrp3 and activation of caspase-1 were increased in PGN+poly(I:C)-treated uterus, which could induce pyroptosis. These results suggest that the double hit of PGN+poly(I:C) induces preterm labor via reduction of a2V expression and simultaneous activation of apoptosis and inflammatory processes.
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