Urine cytokines suggest an inflammatory response in the overactive bladder: a pilot study

Tyagi, Pradeep; Barclay, Derek; Zamora, Rubén; Yoshimura, Naoki; Peters, Kenneth M.; Vodovotz, Yoram; Chancellor, Michael B.

doi:10.1007/s11255-009-9647-5

Cited by 162 publications

(158 citation statements)

References 35 publications

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“…85 Elevated urine cytokines were also found in OAB patients, suggesting an inflammatory component to OAB. 86 Chemokines are chemotactic cytokines that exert their effects through interaction with 7-transmembrane spanning, G protein-coupled receptors, and are present on glycosaminoglycans linked to endothelial cell layers. 87 The most important chemokines causing chemotactic migration of macrophages, eosinophils and mast cells belong to the CC family of chemokines distinguished by adjacent positions of the first two cysteine amino acids.…”

Section: Urinary Proteomics In the Differential Diagnosis Between Oabmentioning

confidence: 99%

Potential urine and serum biomarkers for patients with bladder pain syndrome/interstitial cystitis

Kuo

2014

Int J of Urology

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Abbreviations & Acronyms APF = antiproliferative factor BPS/IC = bladder pain syndrome/interstitial cystitis BUC = bladder urothelial cells CRP = C-reactive protein EGF = epidermal growth factor GP51 = glycoprotein 51 HB-EGF = heparin binding growth factor-like growth factor IC = interstitial cystitis IL = interleukin MCP-1 = monocyte chemotactic protein-1 MIP-1β = macrophage inflammatory protein OAB = overactive bladder NGF = nerve growth factor NIDDK = National Institute of Diabetes, Digestive, and Kidney Diseases TNF-α = tumor necrosis factor-α ZO-1 = zonula occludens-1 Abstract: There is a lack of consensus on the pathophysiology of bladder pain syndrome/ interstitial cystitis. The chronic pain symptoms of bladder pain syndrome/interstitial cystitis refractory to local treatment could be a result of central nervous system sensitization and persisting abnormalities in the bladder wall, which activate the afferent sensory system. Evidence also shows that bladder pain syndrome/interstitial cystitis is a heterogeneous syndrome and that the two subtypes, the ulcerative (classic) and non-ulcerative types, represent different disease entities. There is a need for non-invasive markers for the differential diagnoses of the subtypes of bladder pain syndrome/interstitial cystitis, and between bladder pain syndrome/interstitial cystitis and bladder sensory disorders, such as hypersensitive bladder syndrome or overactive bladder. Bladder pain syndrome/interstitial cystitis, but not overactive bladder, involves an aberrant differentiation program in the bladder urothelium that leads to altered synthesis of several proteoglycans, cell adhesion and tight junction proteins, and bacterial defense molecules. These findings have led to the rationale for identifying urinary biomarkers to detect bladder pain syndrome/interstitial cystitis in patients with frequency urgency syndrome. Recently, the markers that have been the focus of the most research are antiproliferative factor, epidermal growth factor, heparin-binding epidermal growth factor, glycosaminoglycans and bladder nitric oxide. In addition, inflammatory proteins in the urine and serum play important roles in the pathogenesis of bladder pain syndrome/interstitial cystitis. The urinary proteome is an easily accessible source of biomarkers for differentiation between inflammatory bladder disorders. Analysis of multiple urinary proteins and serum cytokines could provide a diagnostic basis for bladder pain syndrome/interstitial cystitis, and could be a tool for the differential diagnosis of bladder pain syndrome/interstitial cystitis and other sensory bladder disorders.

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Section: Urinary Proteomics In the Differential Diagnosis Between Oabmentioning

confidence: 99%

Potential urine and serum biomarkers for patients with bladder pain syndrome/interstitial cystitis

Kuo

2014

Int J of Urology

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“…Bladder biopsies have demonstrated histological evidence of inflammatory changes in OAB in the absence of urinary tract infection [5]. Basic research has implied that bladder inflammation might be augmented and could cause sensitization via the release of chemokines in the suburothelium [3,4]. Gap junction interactions between suburothelial myofibroblasts, urothelium and detrusor smooth muscle cells may be altered by cytokine expression, and OAB can be an inflammatory process in the bladder [3,4].…”

Section: Pol Scientificmentioning

confidence: 99%

“…Basic research has implied that bladder inflammation might be augmented and could cause sensitization via the release of chemokines in the suburothelium [3,4]. Gap junction interactions between suburothelial myofibroblasts, urothelium and detrusor smooth muscle cells may be altered by cytokine expression, and OAB can be an inflammatory process in the bladder [3,4]. The presence of elevated urine cytokine and chemokine levels may support the relationship between inflammation and afferent nerve sensitization [26,27].…”

Section: Pol Scientificmentioning

confidence: 99%

“…Neurotrophins, such as urinary nerve growth factor (NGF), cytokines and chemokines, are associated with morphological changes in sensory and motor neurons that innervate the bladder and contribute to inflammation and afferent sensitization [2,3]. NGF is a well-documented candidate biomarker for OAB, but no correlation of NGF with symptom severity has been reported, and the results of antimuscarinic treatment on NGF are not clear.…”

Section: Introductionmentioning

confidence: 99%

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Data do not support the use of elevated urinary nerve growth factor and fractalkine levels as diagnostic and prognostic biomarkers for women with overactive bladder

Başok

Pelit

et al. 2015

Bladder

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OBJECTIVE: This study investigated urinary nerve growth factor (NGF) and fractalkine levels in women with overactive bladder (OAB), as well as diagnostic and/or prognostic roles, and correlation of these urinary biomarkers with symptom severity of patients. MATERIALS AND METHODS:Twenty-seven women with OAB and 26 healthy subjects were enrolled. Patients were diagnosed with OAB based on symptoms, a 3-day voiding diary and a validated Turkish version of the Overactive Bladder-Validated 8 (OAB-V8) questionnaire. The urinary baseline levels of NGF and fractalkine were compared between OAB patients and control group. The Turkish-validated International Consultation on Incontinence Questionnaire Short Form and OAB-V8 used to categorize patients according to disease severity to assess treatment efficacy. Further urinary NGF and fractalkine levels were compared before and after antimuscarinic treatment. RESULTS:Urinary NGF/creatinine (Cr) and fractalkine/Cr were significantly elevated in OAB patients (0.40 ± 0.40 ng/ mg and 4.63 ± 4.36 ng/mg, respectively) compared to healthy subjects (0.14 ± 0.08 ng/mg and 2.00 ± 1.29 ng/mg, P = 0.002 and P = 0.005, respectively). Sensitivity and specificity were 85.2%, 65.4% for NGF, and 74.1%, 65.4% for fractalkine, respectively. No significant differences in NGF/Cr and fractalkine/Cr compared to baseline (P = 0.063 and 0.162, respectively) were observed after trospium chloride treatment in OAB patients. NGF/Cr and fractalkine/Cr exhibited no correlations with symptom severity levels. CONCLUSIONS:Increased urinary NGF/Cr and fractalkine/Cr levels were found in OAB women. However, the sensitivity and specificity were not sufficient for diagnostic use. NGF and fractalkine levels were decreased after treatment insignificantly, and there was no correlation with symptom severity; therefore their prognostic worth was limited.

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“…In both human and animal models, chronic inflammation of the bladder is closely associated with the characteristics of overactive bladder (OAB) and overactive detrusor [4,5]. It can affect both women and men, although it is more common in women.…”

Section: Introductionmentioning

confidence: 99%

The Association between Chronic Inflammation and Recurrent Cystitis in Women

Chung

2016

Urogenit Tract Infect

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Recurrent urinary tract infection is a common infectious disease seen in the clinic. It is very prevalent in women; as many as 15% of women develop urinary tract infection each year, and at least 25% have one or more recurrences. Chronic inflammation and increased urothelial apoptosis reflect a common pathophysiology in various lower urinary tract dysfunctions, causing bladder storage symptoms. It has been suggested that chronic inflammation could be associated with overactive detrusor and increased levels of urinary nerve growth factor and creatinine. The level of urinary nerve growth factor may decrease after an effective antimuscarinic therapy. Recurrent urinary tract infection could be prevented by using nonsteroidal anti-inflammatory drugs or cyclooxygenase-2 inhibitors. Intravesical hyaluronate and chondroitin sulfate reduce the incidence of recurrent bacterial cystitis, and treatment with hyaluronate targets bacterial adherence to the bladder mucosa in interstitial cystitis/bladder pain syndrome. This article reviews the pathophysiology of chronic inflammation of the bladder and investigates the association between chronic inflammation and recurrent urinary tract infection.

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Urine cytokines suggest an inflammatory response in the overactive bladder: a pilot study

Abstract: The presence of elevated levels in urine of inflammatory biomarkers involved in inflammation and tissue repair suggests a role for inflammation in OAB, and may help in diagnosis and treatment of this disease.

Cited by 162 publications

References 35 publications

Potential urine and serum biomarkers for patients with bladder pain syndrome/interstitial cystitis

Potential urine and serum biomarkers for patients with bladder pain syndrome/interstitial cystitis

Data do not support the use of elevated urinary nerve growth factor and fractalkine levels as diagnostic and prognostic biomarkers for women with overactive bladder

The Association between Chronic Inflammation and Recurrent Cystitis in Women

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