Human Chorionic Gonadotropin Has Anti-Inflammatory Effects at the Maternal-Fetal Interface and Prevents Endotoxin-Induced Preterm Birth, but Causes Dystocia and Fetal Compromise in Mice1
| Autor: | Amapola Balancio, Sonia S. Hassan, Aashna Sahi, Amy Eunice Furcron, Roberto Romero, Nardhy Gomez-Lopez, Claire Nord, Bogdan Panaitescu, Tara N. Mial |
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| Rok vydání: | 2016 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty medicine.medical_treatment Interleukin-1beta Biology Chorionic Gonadotropin Ultrasonography Prenatal Human chorionic gonadotropin Mice 03 medical and health sciences Fetus 0302 clinical medicine Immune system Pregnancy Internal medicine Decidua Leukocytes medicine Animals Progesterone reproductive and urinary physiology 030219 obstetrics & reproductive medicine Estradiol Articles Cell Biology General Medicine medicine.disease Dystocia Endotoxins Mice Inbred C57BL Interleukin 10 030104 developmental biology medicine.anatomical_structure Endocrinology Cytokine Reproductive Medicine Premature Birth Female Tumor necrosis factor alpha hormones hormone substitutes and hormone antagonists |
| Zdroj: | Biology of Reproduction. 94 |
| ISSN: | 1529-7268 0006-3363 |
| DOI: | 10.1095/biolreprod.116.139345 |
| Popis: | Human chorionic gonadotropin (hCG) is implicated in the maintenance of uterine quiescence by down-regulating myometrial gap junctions during pregnancy, and it was considered as a strategy to prevent preterm birth after the occurrence of preterm labor. However, the effect of hCG on innate and adaptive immune cells implicated in parturition is poorly understood. Herein, we investigated the immune effects of hCG at the maternal-fetal interface during late gestation, and whether this hormone can safely prevent endotoxin-induced preterm birth. Using immunophenotyping, we demonstrated that hCG has immune effects at the maternal-fetal interface (decidual tissues) by: 1) increasing the proportion of regulatory T cells; 2) reducing the proportion of macrophages and neutrophils; 3) inducing an M1 → M2 macrophage polarization; and 4) increasing the proportion of T helper 17 cells. Next, ELISAs were used to determine whether the local immune changes were associated with systemic concentrations of progesterone, estradiol, and/or cytokines (IFNgamma, IL1beta, IL2, IL4, IL5, IL6, IL10, IL12p70, KC/GRO, and TNFalpha). Plasma concentrations of IL1beta, but not progesterone, estradiol, or any other cytokine, were increased following hCG administration. Pretreatment with hCG prevented endotoxin-induced preterm birth by 44%, proving the effectiveness of this hormone as an anti-inflammatory agent. However, hCG administration alone caused dystocia and fetal compromise, as proven by Doppler ultrasound. These results provide insight into the mechanisms whereby hCG induces an anti-inflammatory microenvironment at the maternal-fetal interface during late gestation, and demonstrate its effectiveness in preventing preterm labor/birth. However, the deleterious effects of this hormone on mothers and fetuses warrant caution. |
| Databáze: | OpenAIRE |
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