Current medical science · 2026
Multi-Omics Analysis Reveals Inflammatory Activation and Maternal-Fetal Interface Remodeling in Spontaneous Abortion.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Huang Yan-Juan, Shen Zou-Qin-Xuan, Hu Dan-Ping, Huang Ying-Yuan, Chen Guang-Yu, Lin Ying, Hu Bang-Mei, Yuan Xiao-Xiao, Deng Gao-Pi, Li Xing
Аннотация
BACKGROUND: Spontaneous abortion (SA) is a common adverse outcome of early pregnancy, yet its underlying pathophysiological mechanisms remain incompletely understood. Accumulating evidence suggests that dysregulated inflammatory responses at the maternal-fetal interface play a critical role in pregnancy loss. However, the potential associations between alterations in gut microbiota, metabolic disturbances, and localized decidual inflammation in patients with SA have not been systematically characterized.
METHODS: Women with SA (n = 30) and those with normal early pregnancy (NP, n = 28) were enrolled in this study. Proinflammatory cytokines were quantified in decidual tissue homogenates, and histopathological and molecular analyses were performed to evaluate inflammatory activation at the maternal-fetal interface. The gut microbiota composition was profiled using shotgun metagenomic sequencing, while metabolic alterations in the feces were assessed by untargeted metabolomics. Integrated multi-omics analyses were conducted to explore associations among gut microbial dysbiosis, metabolic perturbations, decidual inflammatory signaling, and molecular alterations.
RESULTS: Compared with those from the NP group, the decidual tissues from the SA group exhibited significantly elevated levels of IL-1β and TNF-α (1.49-fold and 1.51-fold, both P < 0.0001), accompanied by pronounced histopathological abnormalities. Enhanced activation of the NF-κB signaling pathway was observed at the maternal-fetal interface in SA patients. Metagenomic analyses revealed distinct differences in the gut microbiota composition and community structure between the two groups, with differentially abundant bacterial taxa identified (LDA score > 2.0). Consistent with these findings, fecal metabolomic profiling clearly revealed differences between SA and NP patients, with differentially abundant metabolites (VIP > 1.0, adjusted P < 0.05) predominantly enriched in lipid metabolism, amino acid metabolism, and immune-related pathways. In addition, the expression of leucine-rich repeat-containing G protein-coupled receptor 6 was significantly upregulated (P < 0.0001) in the decidual tissue of SA patients.
CONCLUSIONS: These findings indicate that SA is associated with localized inflammatory activation at the maternal-fetal interface, dysregulation of decidual molecular activity, gut microbiota dysbiosis, and metabolic perturbations. Integrated multi-omics analyses suggest potential interactions among these factors that may be linked to decidual dysfunction during early pregnancy, providing new insights into the complex pathophysiology of SA.
METHODS: Women with SA (n = 30) and those with normal early pregnancy (NP, n = 28) were enrolled in this study. Proinflammatory cytokines were quantified in decidual tissue homogenates, and histopathological and molecular analyses were performed to evaluate inflammatory activation at the maternal-fetal interface. The gut microbiota composition was profiled using shotgun metagenomic sequencing, while metabolic alterations in the feces were assessed by untargeted metabolomics. Integrated multi-omics analyses were conducted to explore associations among gut microbial dysbiosis, metabolic perturbations, decidual inflammatory signaling, and molecular alterations.
RESULTS: Compared with those from the NP group, the decidual tissues from the SA group exhibited significantly elevated levels of IL-1β and TNF-α (1.49-fold and 1.51-fold, both P < 0.0001), accompanied by pronounced histopathological abnormalities. Enhanced activation of the NF-κB signaling pathway was observed at the maternal-fetal interface in SA patients. Metagenomic analyses revealed distinct differences in the gut microbiota composition and community structure between the two groups, with differentially abundant bacterial taxa identified (LDA score > 2.0). Consistent with these findings, fecal metabolomic profiling clearly revealed differences between SA and NP patients, with differentially abundant metabolites (VIP > 1.0, adjusted P < 0.05) predominantly enriched in lipid metabolism, amino acid metabolism, and immune-related pathways. In addition, the expression of leucine-rich repeat-containing G protein-coupled receptor 6 was significantly upregulated (P < 0.0001) in the decidual tissue of SA patients.
CONCLUSIONS: These findings indicate that SA is associated with localized inflammatory activation at the maternal-fetal interface, dysregulation of decidual molecular activity, gut microbiota dysbiosis, and metabolic perturbations. Integrated multi-omics analyses suggest potential interactions among these factors that may be linked to decidual dysfunction during early pregnancy, providing new insights into the complex pathophysiology of SA.