Characteristics of the vaginal microbiome in women with premature ovarian insufficiency Original paper

What was studied?

This study investigated the premature ovarian insufficiency vaginal microbiome, focusing on how microbial community structure differs between affected women and healthy controls. Using 16S rRNA gene sequencing of V3–V4 regions, the researchers analysed vaginal samples from 28 women with spontaneous premature ovarian insufficiency (POI) and 12 healthy women to determine whether specific microbial shifts were associated with changes in ovarian hormones. The work explored alterations across microbial diversity, taxonomic composition, and predicted metabolic pathways. By integrating sequencing outputs with serum hormone profiles, the researchers mapped relationships between microbial taxa and key reproductive hormones, including estradiol, follicle-stimulating hormone (FSH), luteinizing hormone (LH), and anti-Müllerian hormone (AMH). The study also evaluated metabolic pathway differences using PICRUSt2, identifying shifts in carbohydrate metabolism, ribonucleotide synthesis, and amino acid degradation. These multimodal analyses were designed to clarify whether vaginal microbial signatures reflect systemic hormonal changes in POI and whether specific taxa contribute to the underlying ovarian dysfunction.

Who was studied?

Participants included 40 women aged 24–40 years recruited from Shenzhen Maternity and Child Healthcare Hospital between August and September 2020. Twenty-eight women met diagnostic criteria for spontaneous POI, defined by primary or secondary amenorrhea before age 40 and repeatedly elevated FSH levels above 40 IU/L. Twelve women with regular menstruation and normal FSH levels constituted the control group. Exclusion criteria were comprehensive, removing individuals with recent antibiotic use, pregnancy, autoimmune disease, pelvic surgery, gastrointestinal disorders, metabolic abnormalities, abnormal BMI, smoking, or cancer treatments. All participants provided blood and vaginal secretion samples; hormone levels were assessed via ELISA. Women with POI exhibited markedly higher FSH, LH, testosterone, and FSH/LH ratios and significantly lower estradiol and AMH levels. These differences provided the hormonal context for interpreting microbial shifts observed in sequencing data.

Most important findings

The study revealed substantial compositional and functional microbiome differences in POI. Diversity analyses showed significantly higher weighted UniFrac distances in POI, indicating altered community structure. Taxonomically, the POI group showed pronounced reductions in Lactobacillus, Brevundimonas, and Odoribacter, alongside increased Streptococcus, as confirmed by LDA analysis. Correlation heatmaps showed Lactobacillus positively associated with estradiol and negatively with FSH, aligning reduced Lactobacillus abundance with hallmark POI hormone patterns. Streptococcus displayed the opposite pattern, positively correlating with FSH and LH. Predicted functional differences highlighted 16 significantly altered pathways, including enrichment of pyrimidine salvage and L-arginine degradation pathways in POI. Notably, LACTOSECAT-PWY, a pathway supporting galactose metabolism, was reduced, suggesting potential galactose accumulation and ovarian toxicity.

Key implications

The findings indicate that vaginal microbial dysbiosis is closely linked to hormonal disruption in POI, particularly through loss of Lactobacillus dominance and enrichment of pro-inflammatory taxa such as Streptococcus and Gardnerella. These microbial shifts may contribute to autoimmune activation, impaired mucosal immunity, and altered carbohydrate metabolism, all of which could influence ovarian decline. The study highlights the potential for microbiome-based biomarkers and therapeutic strategies to support early POI detection or intervention.

Citation

Wu J, Ning Y, Tan L, Chen Y, Huang X, Zhuo Y. Characteristics of the vaginal microbiome in women with premature ovarian insufficiency. J Ovarian Res. 2021;14:172. doi:10.1186/s13048-021-00923-9. s13048-021-00923-9