Gut microbiome and endometriosis: a bidirectional interaction

Abstract

Background. Endometriosis is a chronic estrogen-dependent inflammatory disease with a multifactorial pathogenesis. Increasing evidence suggests that the gut microbiome contributes to disease development through interactions involving immune regulation, intestinal barrier integrity, microbial metabolites, and estrogen metabolism, while endometriosis may also alter microbial composition. Aim. To summarize current evidence on the relationship between the gut microbiome and endometriosis, focusing on pathogenic mechanisms, microbial alterations, diagnostic potential, and microbiome-directed therapies. Material and methods. A narrative literature review with a structured search strategy was conducted using PubMed, Embase, the Cochrane Library, and Google Scholar. Search terms included endometriosis, gut microbiome, dysbiosis, estrobolome, intestinal permeability, inflammation, oxidative stress, probiotics, and fecal microbiota transplantation. Results. Current evidence supports a bidirectional relationship between gut dysbiosis and endometriosis. Microbial alterations may promote immune dysregulation, increased intestinal permeability, oxidative stress, lipopolysaccharide-mediated inflammation, and enhanced estrogen recirculation via the estrobolome, facilitating lesion establishment and persistence. Conversely, chronic inflammation, hormonal treatment, surgery, and bowel involvement may further modify the gut microbiome. Although no consistent microbial signature has been identified, several taxa and functional pathways have been associated with disease phenotype and severity. Conclusions. The gut microbiome is an important modifier of endometriosis rather than a single causative factor. Microbiome-derived biomarkers and targeted therapies show promise but require validation in prospective studies before routine clinical use.