Gut microbiota imbalance and its correlations with hormone and inflammatory factors in patients with stage 3/4 endometriosis Original paper

What Was Studied?

This study explored the associations between gut microbiota imbalances and hormone and inflammatory factors in patients with stage 3/4 endometriosis (EM). Conducted at Changhai Hospital, Shanghai, the research aimed to determine how gut microbiome alterations correlate with hormone levels and inflammatory markers in women suffering from moderate to severe endometriosis. Using 16S rRNA high-throughput sequencing, researchers analyzed stool samples to compare the gut microbial composition between 12 women diagnosed with stage 3/4 EM and 12 healthy controls. Blood samples were collected to measure serum hormone levels, including estradiol (E2), and inflammatory cytokines, notably IL-8. The primary objective was to identify microbial shifts associated with EM and understand their correlation with hormone imbalances and inflammation, key factors in the pathogenesis of endometriosis.

Who Was Studied?

The study recruited 12 women with a histological diagnosis of stage 3/4 endometriosis from Changhai Hospital and 12 healthy controls, matched for age (18–40 years) and menstrual regularity. Inclusion criteria for the EM group required confirmed diagnoses of moderate to severe endometriosis per the American Fertility Society Revised Classification (1997). All participants were Han women living in Shanghai, with strict exclusion criteria including recent antibiotic or probiotic use, hormonal therapy, pregnancy, and any comorbid gastrointestinal conditions like inflammatory bowel disease. To minimize confounding factors, participants followed a uniform carbohydrate-based diet three days before sampling, and stool samples were collected within three to five days post-menstruation to account for hormonal fluctuation.

What Were the Most Important Findings?

The study found that women with stage 3/4 endometriosis exhibited a significantly altered gut microbiota profile compared to healthy controls. Notably, the EM group had lower α diversity, indicating reduced microbial richness and variation. At the phylum level, the ratio of Firmicutes to Bacteroidetes was markedly increased in endometriosis patients (3.55 vs. 1.99 in controls), suggesting dysbiosis. The abundance of Actinobacteria, Cyanobacteria, Saccharibacteria, Fusobacteria, and Acidobacteria was significantly higher in the EM group, while Tenericutes were significantly reduced. At the genus level, Bifidobacterium, Blautia, Dorea, Streptococcus, and [Eubacterium] hallii_group showed notable increases, whereas Lachnospira and [Eubacterium] eligens_group were depleted in endometriosis patients. Among the unique genera, Prevotella_7 dominated the EM group, while Coprococcus_2 was prevalent in controls.

Additionally, serum analyses revealed that estradiol (E2) and IL-8 levels were significantly higher in endometriosis patients. Correlation analysis indicated that Blautia and Dorea were positively correlated with elevated E2 levels, while Subdoligranulum abundance inversely correlated with IL-8 levels. These microbial shifts also corresponded with enhanced expression of microbial pathways related to “environmental information processing,” “endocrine system,” and “immune system,” highlighting potential links between gut microbiota and hormonal regulation in endometriosis.

What Are the Greatest Implications of This Study?

The findings of this study suggest that gut microbiota imbalances are closely linked with hormone and inflammatory dysregulation in patients with stage 3/4 endometriosis. The observed microbial shifts, particularly the elevated Firmicutes/Bacteroidetes ratio and increased levels of Bifidobacterium, Blautia, Dorea, and Streptococcus, indicate a state of dysbiosis that may exacerbate inflammatory responses and hormonal imbalances. The positive correlation between Blautia and Dorea with estradiol levels points to the gut microbiome’s role in modulating estrogen, potentially influencing the development and progression of endometriosis. Furthermore, the association of Subdoligranulum with IL-8 levels suggests a microbial influence on inflammatory cytokine production, which is known to contribute to endometriosis pathophysiology. These insights provide a foundation for exploring microbiome-targeted therapies aimed at restoring microbial balance and modulating hormonal and inflammatory responses in endometriosis patients. This study also underscores the need for further clinical investigations to validate these microbial markers as diagnostic or therapeutic targets.