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Supporting this model, peripheral blood mononuclear cells from women with chronic pelvic pain release significantly greater amounts of IL-1 following lipopolysaccharide-induced TLR4 activation, compared with pain-free controls, indicating a state of peripheral immune hyper-responsiveness and systemic neuroimmune sensitization ( versus ectopic tissue implantation (Tsamantioti and Mahdy, 2025), both disorders exhibit abnormal endometrial progesterone signaling and chronic inflammatory signaling that may converge on a shared neuroimmune axis driving pelvic pain ( 4.5 Oxidative stress and pain sensitization There is growing evidence that oxidative stress may be involved in the multifactorial pathophysiology of PCOS, as it can synergize with heightened levels of basal proinflammatory signaling molecules to worsen the disease (Zeber-Lubecka et al., 2023)

This immunosuppression may be associated with increased susceptibility to viral, protozoal, and fungal infections

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