Research progress in the correlation between reproductive tract microbiota and intrauterine adhesion
- PMID: 36481627
- PMCID: PMC10930615
- DOI: 10.11817/j.issn.1672-7347.2022.220130
Research progress in the correlation between reproductive tract microbiota and intrauterine adhesion
Abstract
Intrauterine adhesion (IUA) is caused by damage of the basal layer of endometrium, which leads to fibrosis of the endometrium and the formation of adhesion, resulting in partial or complete occlusion of the uterine cavity, abnormal menstruation, infertility or recurrent miscarriage. The prevalence of IUA in women has been increasing in recent years, and the high recurrence rate of moderate to severe IUA makes IUA treatment more challenging. Iatrogenic endometrial injury is the main cause of IUA. However, the incidence of IUA and the severity of IUA vary among patients who have received similar uterine operations, suggesting that there may be other synergistic factors in the development of IUA. There is a certain correlation between the pathogenesis and the microbiota of the gential tract. In many IUA patients, it has been observed that the probiotics such as Lactobacillus in the vagina is significant reduced, and the pathogenic bacteria such as Gardnerella and Prevotella are excessive growth. The reproductive tract microbiota can be involved in the development and progression of IUA via impacting immune function and metabolism.
宫腔粘连(intrauterine adhesion,IUA)是由于子宫内膜基底层受损导致内膜纤维化形成粘连,以致宫腔部分或全部闭塞,从而导致月经异常、不孕或反复流产。近年来IUA患病率呈上升趋势,且中重度IUA的高复发率使IUA治疗更具挑战性。医源性子宫内膜损伤是IUA的主要病因,但在临床上接受过类似宫腔操作的患者中,IUA发病与否以及IUA的严重程度也不尽相同,因此IUA的发生可能存在其他的协同作用因素。IUA发病机制与生殖道微生物群存在一定的关联性,在许多IUA患者中都观察到阴道内乳杆菌等益生菌显著减少,加德纳菌和普雷沃氏菌等病原菌过度生长。生殖道微生物群能通过影响免疫功能和代谢来参与IUA的发生和发展。.
Keywords: cytokine; immune response; intrauterine adhesion; reproductive tract microbiota.
Conflict of interest statement
作者声称无任何利益冲突。
Figures

Similar articles
-
Deep Grouping Analysis of the Altered Cervical Canal Microbiota in Intrauterine Adhesion Patients.Reprod Sci. 2022 Dec;29(12):3494-3507. doi: 10.1007/s43032-022-01006-w. Epub 2022 Jun 16. Reprod Sci. 2022. PMID: 35710962
-
Study on the correlation among dysbacteriosis, imbalance of cytokine and the formation of intrauterine adhesion.Ann Transl Med. 2020 Feb;8(4):52. doi: 10.21037/atm.2019.11.124. Ann Transl Med. 2020. PMID: 32175346 Free PMC article.
-
Revealing the interaction between intrauterine adhesion and vaginal microbiota using high‑throughput sequencing.Mol Med Rep. 2019 May;19(5):4167-4174. doi: 10.3892/mmr.2019.10092. Epub 2019 Mar 27. Mol Med Rep. 2019. PMID: 30942434 Free PMC article.
-
Intrauterine adhesion.Taiwan J Obstet Gynecol. 2024 May;63(3):312-319. doi: 10.1016/j.tjog.2024.02.004. Taiwan J Obstet Gynecol. 2024. PMID: 38802193 Review.
-
Treatment strategies for intrauterine adhesion: focus on the exosomes and hydrogels.Front Bioeng Biotechnol. 2023 Aug 31;11:1264006. doi: 10.3389/fbioe.2023.1264006. eCollection 2023. Front Bioeng Biotechnol. 2023. PMID: 37720318 Free PMC article. Review.
Cited by
-
Growth hormone combined with estrogen improves intrauterine adhesion fibrosis by downregulating endometrial microbial citraconic acid to target β-catenin protein.mSystems. 2025 Jul 22;10(7):e0169224. doi: 10.1128/msystems.01692-24. Epub 2025 Jun 5. mSystems. 2025. PMID: 40470939 Free PMC article.
References
-
- 付青, 卢秀琴, 王延明, 等. 宫腔粘连分子机制的研究进展[J]. 临床与实验病理学杂志, 2019, 35(9): 1079-1081. 10.13315/j.cnki.cjcep.2019.09.015. - DOI
- FU Qing, LU Xiuqin, WANG Yanming, et al. . Research progress on molecular mechanism of intrauterine adhesion[J]. Chinese Journal of Clinical and Experimental Pathology, 2019, 35(9): 1079-1081. 10.13315/j.cnki.cjcep.2019.09.015. - DOI
-
- 靳灵鸽, 李珊珊, 郑萍, 等. 宫腔粘连组织中TLR4/NF-κB通路功能改变与细胞因子分泌、胶原代谢特征的相关性[J]. 海南医学院学报, 2019, 25(1): 33-36. 10.13210/j.cnki.jhmu.20181204.001. - DOI
- JIN Lingge, LI Shanshan, ZHENG Ping, et al. . Correlation of changes of TLR4/NF-κB pathway function in intrauterine adhesion tissue with characteristics of cytokine secretion and collagen metabolism[J]. Journal of Hainan Medical University, 2019, 25(1): 33-36. 10.13210/j.cnki.jhmu.20181204.001. - DOI
MeSH terms
Grants and funding
LinkOut - more resources
Full Text Sources