The association of gut microbiome with recurrent pregnancy loss: A comprehensive review

被引:4
|
作者
Zhu, Jun [1 ]
Jin, Jiaxi [1 ]
Qi, Qing [2 ,3 ,4 ]
Li, Lisha [2 ,3 ,4 ]
Zhou, Jing [2 ,3 ,4 ]
Cao, Liwen [5 ]
Wang, Ling [2 ,3 ,4 ,6 ]
机构
[1] Wenzhou Med Univ, Affiliated Wenling Hosp, Wenzhou, Zhejiang, Peoples R China
[2] Fudan Univ, Lab Reprod Immunol Obstet & Gynecol Hosp, Shanghai, Peoples R China
[3] Fudan Univ, Acad Integrat Med, Shanghai, Peoples R China
[4] Shanghai Key Lab Female Reprod Endocrine Related D, Shanghai, Peoples R China
[5] Zhoushan Women & Children Hosp, Ctr Reprod Med, Hangzhou, Zhejiang, Peoples R China
[6] Fudan Univ, Lab Reprod Immunol Obstet & Gynecol Hosp, 419 Fangxie Rd, Shanghai 200011, Peoples R China
关键词
gut microbiome; recurrent pregnancy loss; inflammation; insulin resistance; immunity; obesity; DIET-INDUCED OBESITY; INSULIN-RESISTANCE; FATTY-ACIDS; INFLAMMATION; BUTYRATE; CELLS; MISCARRIAGE; SENSITIVITY; BACTERIAL; DISEASE;
D O I
10.5582/ddt.2023.01010
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The steady-state gut microbiome not only promotes the metabolism and absorption of nutrients that are difficult to digest by the host itself, but also participates in systemic metabolism. Once the dynamic balance is disturbed, the gut microbiome may lead to a variety of diseases. Recurrent pregnancy loss (RPL) affects 1-2% of women of reproductive age, and its prevalence has increased in recent years. According to the literature review, the gut microbiome is a new potential driver of the pathophysiology of recurrent abortion, and the gut microbiome has emerged as a new candidate for clinical prevention and treatment of RPL. However, few studies have concentrated on the direct correlation between RPL and the gut microbiome, and the mechanisms by which the gut microbiome influences recurrent miscarriage need further investigation. In this review, the effects of the gut microbiome on RPL were discussed and found to be associated with inflammatory response, the disruption of insulin signaling pathway and the formation of insulin resistance, maintenance of immunological tolerance at the maternal-fetal interface due to the interference with the immune imbalance of Treg/Th17 cells, and obesity.
引用
收藏
页数:13
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