Tang Fan, Deng Mengqi, Xu Chunyu, Yang Ruiye, Ji Xuechao, Hao Menglin, Wang Yixiao, Tian Ming, Geng Yuning, Miao Jinwei
Department of Gynecologic Oncology, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital, Beijing, China.
Front Cell Infect Microbiol. 2024 Feb 16;14:1328419. doi: 10.3389/fcimb.2024.1328419. eCollection 2024.
Endometriosis (EMs) is a prevalent gynecological disorder characterized by the growth of uterine tissue outside the uterine cavity, causing debilitating symptoms and infertility. Despite its prevalence, the exact mechanisms behind EMs development remain incompletely understood. This article presents a comprehensive overview of the relationship between gut microbiota imbalance and EMs pathogenesis. Recent research indicates that gut microbiota plays a pivotal role in various aspects of EMs, including immune regulation, generation of inflammatory factors, angiopoietin release, hormonal regulation, and endotoxin production. Dysbiosis of gut microbiota can disrupt immune responses, leading to inflammation and impaired immune clearance of endometrial fragments, resulting in the development of endometriotic lesions. The dysregulated microbiota can contribute to the release of lipopolysaccharide (LPS), triggering chronic inflammation and promoting ectopic endometrial adhesion, invasion, and angiogenesis. Furthermore, gut microbiota involvement in estrogen metabolism affects estrogen levels, which are directly related to EMs development. The review also highlights the potential of gut microbiota as a diagnostic tool and therapeutic target for EMs. Interventions such as fecal microbiota transplantation (FMT) and the use of gut microbiota preparations have demonstrated promising effects in reducing EMs symptoms. Despite the progress made, further research is needed to unravel the intricate interactions between gut microbiota and EMs, paving the way for more effective prevention and treatment strategies for this challenging condition.
子宫内膜异位症（EMs）是一种常见的妇科疾病，其特征是子宫组织在子宫腔外生长，导致使人衰弱的症状和不孕。尽管其发病率很高，但EMs发生的确切机制仍未完全了解。本文全面概述了肠道微生物群失衡与EMs发病机制之间的关系。最近的研究表明，肠道微生物群在EMs的各个方面都起着关键作用，包括免疫调节、炎症因子的产生、血管生成素的释放、激素调节和内毒素的产生。肠道微生物群的失调会破坏免疫反应，导致炎症和子宫内膜碎片免疫清除受损，从而导致子宫内膜异位病变的发展。失调的微生物群会导致脂多糖（LPS）的释放，引发慢性炎症并促进异位子宫内膜的黏附、侵袭和血管生成。此外，肠道微生物群参与雌激素代谢会影响雌激素水平，而雌激素水平与EMs的发展直接相关。该综述还强调了肠道微生物群作为EMs诊断工具和治疗靶点的潜力。粪便微生物群移植（FMT）和使用肠道微生物群制剂等干预措施已显示出在减轻EMs症状方面有良好效果。尽管取得了进展，但仍需要进一步研究来阐明肠道微生物群与EMs之间复杂的相互作用，为这种具有挑战性的疾病制定更有效的预防和治疗策略铺平道路。
