The Vaginal Microbiome in Health and Disease—What Role Do Common Intimate Hygiene Practices Play? Original paper

What was reviewed?

This paper is a comprehensive narrative review that examined the vaginal microbiome as a central regulator of vaginal health, reproductive outcomes, and susceptibility to infection and inflammation. The authors synthesized microbiological, immunological, and clinical evidence to explain how vaginal microbial communities interact with epithelial barriers, innate immune signaling, and hormonal cycles to maintain a low-inflammatory, pathogen-resistant environment. The review emphasized that the vaginal microbiome is uniquely structured compared with other body sites, with dominance by specific lactic acid–producing bacteria representing an evolved host–microbe partnership rather than a generic feature of microbial diversity. The paper also explored how disruption of this ecosystem contributes to gynecologic and obstetric disease across the lifespan.

Who was reviewed?

The review drew on data from diverse human populations, including healthy reproductive-age women, pregnant individuals, postmenopausal women, adolescents, and patients with vaginal dysbiosis–associated conditions. Clinical cohorts included women with bacterial vaginosis, vulvovaginal candidiasis, sexually transmitted infections, infertility, preterm birth, pelvic inflammatory disease, and increased HIV acquisition risk. These findings were supported by longitudinal cohort studies, metagenomic analyses, in vitro epithelial models, and limited animal data, allowing the authors to integrate microbial composition with immune and clinical outcomes.

What were the most important findings?

The review established that vaginal health is most consistently associated with microbiomes dominated by Lactobacillus species, particularly Lactobacillus crispatus, Lactobacillus jensenii, Lactobacillus gasseri, and Lactobacillus iners. These organisms maintain a low vaginal pH through lactic acid production, suppress pathogen growth, and modulate immune signaling to favor tolerance rather than inflammation. The authors emphasized that lactic acid, rather than hydrogen peroxide alone, is the key antimicrobial and immunomodulatory molecule, reinforcing epithelial tight junctions, reducing pro-inflammatory cytokine expression, and inhibiting viral and bacterial pathogens. In contrast, dysbiotic states such as bacterial vaginosis were characterized by reduced Lactobacillus dominance and increased abundance of anaerobes including Gardnerella vaginalis, Atopobium vaginae, Prevotella, Mobiluncus, and Sneathia.

These communities increased vaginal pH, produced proteases and biogenic amines, disrupted mucus and epithelial barriers, and triggered innate immune activation through Toll-like receptor signaling. The review also highlighted important population-level variation, noting that some asymptomatic women harbor non–Lactobacillus-dominated communities yet maintain relative health, underscoring the need for context-specific interpretation. Importantly, the authors linked vaginal dysbiosis to systemic consequences, including increased risk of preterm birth, heightened HIV susceptibility through mucosal inflammation, and altered reproductive outcomes.

What are the greatest implications of this review?

For clinicians, this review reinforces that vaginal health depends on functional microbial ecology rather than simple pathogen absence. It supports diagnostic and therapeutic strategies that prioritize restoration of protective Lactobacillus-dominated communities and reduction of inflammation, rather than repeated broad-spectrum antimicrobial use that destabilizes microbial resilience and increases recurrence risk.