Yoga and Neuroimmune Modulation in Chronic Pelvic Pain Syndrome: Inflammatory Biomarkers, Central Sensitization, and Pain Phenotypes—A Narrative Review

Background: Chronic pelvic pain syndrome (CPPS) is a heterogeneous, multisystem pain condition characterised by persistent pelvic pain with variable urogenital, bowel, sexual, and psychosocial symptoms. Accumulating evidence indicates that many patients exhibit neuroimmune activation (local and systemic inflammatory signalling) together with nociplastic features driven by central sensitization. Aim: To synthesise mechanistic and clinical evidence on how yoga may alleviate CPPS through neuroimmune modulation—particularly inflammatory pathways and central sensitization—and to outline a phenotype-informed framework for future research and clinical translation. Narrative Review Method: We conducted a narrative review of peer‑reviewed human studies and key mechanistic literature indexed in PubMed, Scopus, Web of Science, and Google Scholar (2000–2025). Evidence was synthesised thematically across (i) CPPS phenotypes and pain mechanisms, (ii) inflammatory biomarkers and neuroimmune pathways, (iii) central sensitization and autonomic–HPA axis dysregulation, and (iv) clinical trials of yoga and closely related mind–body interventions in pelvic pain. Key Findings: CPPS is associated with altered immune–inflammatory profiles (e.g., chemokines/cytokines, neurotrophins such as nerve growth factor, and oxidative stress markers) and with central pain amplification reflected in widespread hyperalgesia, symptom clustering, and comorbidity with chronic overlapping pain conditions. Yoga plausibly targets these mechanisms via vagal–autonomic regulation, reduced HPA-axis hyperarousal, improved affective regulation, and downstream suppression of pro‑inflammatory transcriptional programs. Direct pelvic pain trials of yoga are limited but suggest improvements in pain intensity and quality of life; related evidence from urological pelvic pain, bladder pain syndrome, and central sensitivity syndromes supports benefits on stress reactivity, pain catastrophizing, sleep, and inflammatory signalling. Clinical Implications: A phenotype‑guided yoga prescription—mapping clinical presentation (visceral, pelvic floor myofascial, neuropathic, and nociplastic/centralized features) to targeted yoga components (gentle asana, diaphragmatic breathing, relaxation, and meditation)—may optimize responsiveness and enable biomarker‑informed monitoring. Conclusion: Yoga has strong mechanistic plausibility as an adjunct therapy for CPPS by modulating neuroimmune activation and central sensitization. Robust, adequately powered trials integrating pain phenotyping, autonomic metrics, and inflammatory biomarkers are required to define responders and mechanisms of action.