Microbiome and chronic pelvic pain in women: a mini-review

Abstract Chronic pelvic pain (CPP) is a prevalent, disabling syndrome encompassing overlapping disorders such as endometriosis/adenomyosis, bladder pain syndrome/interstitial cystitis, irritable bowel syndrome, vulvodynia, and myofascial pain syndrome. Despite distinct clinical phenotypes, these conditions converge on shared biological axes—immune dysregulation, endocrine imbalance, and central sensitization—that sustain chronic pain. Increasing evidence implicates the human microbiome as a potential upstream regulator of these pathways. Dysbiosis across the gut, vaginal, urinary, and endometrial microbial ecosystems may promote local and systemic inflammation, compromise epithelial barrier integrity, alter estrogen recirculation through the estrobolome, and engage aberrant neuroimmune signalling along gut–brain and hypothalamic–pituitary–ovarian circuits. Recent multi-site profiling suggests that microbial alterations often co-occur across pelvic compartments but remain anatomically distinct, with shifts in anaerobic taxa and paired cervicovaginal immune signatures supporting microbiome–immune interactions in CPP pathophysiology. This narrative review synthesizes observational, multi-omics, and mechanistic evidence linking microbial dysbiosis to CPP, highlights microbial metabolites as key functional mediators, and evaluates causal data from experimental models. Finally, it discusses translational opportunities and limitations, including microbiome-targeted interventions (dietary modulation, probiotics/psychobiotics, postbiotics, and microbiota transfer approaches) and the need for harmonized, longitudinal and biomarker-embedded trials to enable mechanism-based stratification and rational therapeutic development.