Inflammation may accentuate age-related bladder function decline

May 12 2014

By Joanna Lyford, Senior medwireNews Reporter

Age-associated biochemical changes in the bladder may accentuate the inflammation associated with overactive bladder (OAB), study findings indicate.

Writing in International Urology and Nephrology, the study authors say that urinary levels of certain chemokines “can serve as surrogate markers for monitoring age-associated biochemical changes and the effect of therapeutic interventions in OAB patients.”

Pradeep Tyagi (University of Pittsburgh, Pennsylvania, USA) and colleagues in the USA and Taiwan obtained urine specimens from 140 men and women aged between 25 and 90 years. All were attending a urology clinic for the management of OAB.

Immunoassays were used to test the urine samples for levels of eight chemokines. This included two cytokines (interleukin [IL]-1b and IL-1 receptor antagonist), a CC chemokine (monocyte chemotactic protein-1 [MCP-1]), three CXC chemokines (CXCL1, CXCL8, CXCL10, otherwise known as growth-related oncogene GRO-alpha, IL-8, and interferon gamma-induced protein (IP) 10, respectively) and two growth factors (nerve growth factor [NGF] and platelet-derived growth factor).

None of the proteins were uniformly detected in all the patients, say the authors, which “likely reflects the heterogeneity of OAB in this cohort and different proteins responsible for the varying degree of low-grade inflammation associated with OAB.”

However, levels of three proteins – NGF, MCP-1 and CXCL1 – were significantly and positively associated with age, with Pearson r-values of 0.274, 0.168 and 0.284, respectively. Additionally, OAB symptoms were significantly associated with age, with an odds ratio of 1.12.

Taken together, these findings support the hypothesis that age-related biochemical changes in bladder tissue can be tracked by studying the age-associated changes in urinary proteins, say the authors.

They suggest that elevated NGF in patients with OAB may be a homeostatic response to counter the age-related dendritic, synaptic and axonal degeneration or senescence in the bladder, while age-related elevations in urinary MCP-1 may reflect bladder tissue remodelling.

Meanwhile, CXCL1 is involved in neuroimmune interactions and has been shown to promote neuronal release of calcitonin gene-related peptide. Elevations in this protein may be indicative of an infected or inflamed urinary tract rather than related to OAB, Tyagi et al say.

They conclude: “[C]hronic exposure to inflammatory mediators with progressing age leads to alterations in multiple physiological systems and it may partly explain age-related decline in voiding function. Further studies involving asymptomatic controls are warranted to investigate this phenomenon further.”

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