ArticleAmerican journal of reproductive immunology (New York, N.Y. : 1989)2019
Intrauterine inhibition of chemokine receptor 4 signaling modulates local and systemic inflammation in ovine pregnancy.
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 5 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Placental insufficiency and heavier placentas in sheep after suppressing CXCL12/CXCR4 signaling during implantation†.Biology of reproduction · 2023Article
- Maternal CXCR4 deletion results in placental defects and pregnancy loss mediated by immune dysregulation.JCI insight · 2023Article
- Role of chemokines in early pregnancy loss.Experimental and therapeutic medicine · 2022Article
- CXCL12 May Drive Inflammatory Potential in the Ovine Corpus Luteum During Implantation.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- Inhibition of the C-X-C Motif Chemokine 12 (CXCL12) and Its Receptor CXCR4 Reduces Utero-Placental Expression of the VEGF System and Increases Utero-Placental Autophagy.Frontiers in veterinary science · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
problemChemokines help coordinate inflammation within the fetal-maternal microenvironment during gestation. The chemokine CXCL12 signaling through its receptor CXCR4 regulates inflammatory activity, but this phenomenon is not well understood during pregnancy, and there are no reports exploring the role of this pair in peripheral immune tolerance during gestation. Herein, we hypothesize that intrauterine CXCL12-CXCR4 signaling governs local and systemic immunomodulatory dynamics during early gestation in ewes. METHOD OF STUDY: Osmotic pumps were surgically installed for intrauterine infusion of a CXCR4 inhibitor, AMD3100, beginning on day 12 post-breeding in sheep. Endometrial tissues were collected on day 35 of gestation and evaluated for inflammatory potential, Akt pathway activation, and autophagy induction. Demonstrative of peripheral immune activity, levels of select cytokines were assessed in daily blood samples collected throughout the study, as well as in corpus luteum and spleen on day 35.
resultsAnti-inflammatory IL10 was primarily localized to endometrial glandular epithelium with lower abundance when CXCR4 was antagonized. Inhibition of CXCR4 at the fetal-maternal interface resulted in less activation of Akt in endometrium, while evidence of autophagy induction was greater. Corpora lutea from ewes receiving intrauterine AMD3100 exhibited lower interferon-gamma (IFNG) expression. Blood inflammatory potential was differentially altered in a temporal fashion throughout infusion. IL10 abundance in spleen was greater following CXCR4 inhibition at the fetal-maternal interface, while IFNG was less.
conclusionIntrauterine CXCL12-CXCR4 signaling governs endometrial and systemic inflammation; disruption of this axis may have detrimental impacts on offspring and maternal health.
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Registered trials
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