Unraveling the microbial puzzle: exploring the intricate role of gut microbiota in endometriosis pathogenesis

Front Cell Infect Microbiol. 2024 Feb 16:14:1328419. doi: 10.3389/fcimb.2024.1328419. eCollection 2024.

Abstract

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.

Keywords: endometriosis; gut microbiota; immune; inflammatory; lipopolysaccharide.

Publication types

  • Review

MeSH terms

  • Endometriosis* / etiology
  • Estrogens
  • Female
  • Gastrointestinal Microbiome*
  • Humans
  • Inflammation
  • Microbiota*

Substances

  • Estrogens

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This research was funded by National Natural Science Foundation of China, Grant no. 81771549 Jinwei Miao. Beijing Hospitals Authority’s Clinical Medicine Development of Special Funding Support, Grant no. ZYLX202120 Jinwei Miao. Beijing Hospitals Authority’s Ascent Plan, Grant no. DFL20221201.