Introduction and hypothesis We hypothesize that overactive bladder (OAB) can produce inflammatory cytokines due to afferent neural plasticity or urothelial dysfunction. This study aimed to detect abnormal cytokine levels in urine of patients with OAB compared to urinary tract infections (UTI) and controls. Methods This was a prospective, single blind study including 20 premenopausal women (control), 20 with OAB and 16 with UTI. Urine samples were collected, centrifuged, and stored (?80°C). Urinary total proteins were quantified and detected by antibody-based array chip for release of 120 human cytokines in the two groups relative to the controls. Results Majority of cytokines showed the same expression in the OAB compared with the controls. Cytokines exclusively expressed in OAB were: monocyte chemoattractant protein (MCP) 1, TARC, PARC, and Fas/ TNFRSF6. MCP-2, MCP-3, tumor necrosis factor-β, GCSF and eotaxin-3 showed a shared expression in UTI and OAB. Conversely, few of the cytokines were downregulated in OAB (IL-5, IL-6, IL-7, and GM-CSF). Conclusions Taken together, the results suggest that a subset of inflammatory cytokines and chemokines provides a framework for development of highly optimized urinary biomarker assay for differential diagnosis and treatment of OAB.
- Overactive bladder
- Protein array