Urinary IL-33 and galectin-3 increase in patients with interstitial cystitis/bladder pain syndrome (review).

Interstitial cystitis/bladder pain syndrome (IC/BPS) is an enigmatic chronic disorder characterized by vague bladder pain of variable severity accompanied by urinary symptoms. The pathogenesis and etiology of IC/BPS remain incompletely defined. However, there is an emerging consensus about the central role of epithelial dysfunction, bladder sensory nerve up-regulation, and mast cell activation in the genesis of IC/BPS. Accumulating evidences have suggested that tissue damage is recognized at the cell level via receptor-mediated detection of intracellular proteins (so-called alarmins) released by the necrotic cells. Among these proteins IL-33, galectin-3 (Gal-3) and advanced glycation end products (AGE), may have an important role because they can be participated as cellular components that stimulate the immune system. We determined IL-33, Gal-3, and AGE in 24-hour urine specimens from patients with IC/BPS and healthy subjects. Study participants included 43 woman with IC/BPS and 29 female volunteers. Urinary IL-33, EGF and Gal-3 levels were measured using an enzyme-linked immunosorbent assay, whereas the content of AGE was quantified by natural AGE-specific fluorescence (Ex. 370 nm, Em. 440 nm). Urinary IL-33, and Gal-3 levels were normalized by urinary creatinine (Cr) levels and compared among subgroups. We have found that the levels of IL-33 and Gal-3 were significantly increased in IC/BPS. The level of the IL-33 in the urine of healthy women was equal to 0.32, while the level of IL-33 in IC/BPS patients increases up to 0.58 (p<0.05). Further, the amounts of urine Gal-3 were also elevated in IC/BPS compared to healthy subjects (0.16 versus 0.07; p>0.01) and AGE-specific fluorescence in urine was increased up to 140% in IC/BPS patients. These data suggest on the participation of IL-33, Gal-3 and AGE in the pathogenesis of IC/BPS.