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
- PMID: 39575516
- DOI: 10.1111/aji.70016
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
Abstract
Problem: Intrauterine infection is one of the most jeopardizing conditions associated with adverse outcomes, including preterm birth; however, multiple tolerance mechanisms operate at the maternal-fetal interface to avoid the rejection of the fetus. Among the factors that maintain the uterus as an immunoprivileged site, Galectin-1 (Gal-1), an immunomodulatory glycan-binding protein secreted by the maternal-fetal unit, is pivotal in promoting immune cell homeostasis. This work aimed to evaluate the role of Gal-1 during a lipopolysaccharide (LPS)-induced-inflammatory milieu.
Method of study: Using an ex vivo culture with two independent compartments, human fetal membranes at term were pretreated with 40 and 80 ng/mL of Gal-1, then to reproduce an intraamniotic inflammation, the fetal side of membranes was stimulated with 500 ng/mL of LPS for 24 h. The concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, monocyte chemoattractant protein (MCP1), macrophage inflammatory protein (MIP1) α, regulated upon activation normal T cell expressed and secreted (RANTES), and matrix metalloproteinase (MMP)-9 were measured in both amnion and choriodecidua compartments.
Results: In a tissue-specific fashion profile, pretreatment with the physiologic concentration of Gal-1 significantly diminished the LPS-dependent secretion of TNF-α, IL-1β, Il-6, MCP1, MIP1α, RANTES, and MMP-9.
Conclusion: Gal-1 elicits an anti-inflammatory effect on the human fetal membranes stimulated with LPS, which supports the hypothesis that Gal-1 is part of the immunomodulatory mechanisms intended to stop the harmful effect of inflammation of the maternal-fetal interface.
Keywords: galectin‐1; human chorioamniotic membranes; inflammation; intraamniotic infection; maternal‐fetal unit; preterm birth; preterm labor; tolerogenic.
© 2024 The Author(s). American Journal of Reproductive Immunology published by John Wiley & Sons Ltd.
References
-
- E. O. Ohuma, A. B. Moller, E. Bradley, et al., “National, Regional, and Global Estimates of Preterm Birth in 2020, With Trends From 2010: A Systematic Analysis,” Lancet 402, no. 10409 (2023): 1261–1271, https://doi.org/10.1016/S0140‐6736(23)00878‐4.
-
- J. Perin, A. Mulick, D. Yeung, et al., “Global, Regional, and National Causes of Under‐5 Mortality in 2000–19: An Updated Systematic Analysis With Implications for the Sustainable Development Goals,” Lancet Child Adolesc Health 6, no. 2 (2022): 106–115, https://doi.org/10.1016/S2352‐4642(21)00311‐4.
-
- Secretaria de Salud. Cada Año Nacen En México 200 Mil Bebés Prematuros: Secretaría de Salud. 2022. Accessed July 29, 2024. https://www.gob.mx/salud/prensa/558‐cada‐ano‐nacen‐en‐mexico‐200‐mil‐beb....
-
- R. Menon and L. S. Richardson, “Preterm Prelabor Rupture of the Membranes: A Disease of the Fetal Membranes,” Seminars in Perinatology 41, no. 7 (2017): 409–419, https://doi.org/10.1053/j.semperi.2017.07.012.
-
- W. L. Lee, W. H. Chang, and P. H. Wang, “Risk Factors Associated with Preterm Premature Rupture of Membranes (PPROM),” Taiwanese Journal of Obstetrics and Gynecology 60, no. 5 (2021): 805–806, https://doi.org/10.1016/j.tjog.2021.07.004.