Increased Pro-Inflammatory Cytokines, C-Reactive Protein and Nerve Growth Factor Expressions in Serum of Patients with Interstitial Cystitis/Bladder Pain Syndrome

Jiang, Yuan‐Hong; Peng, Chung-Hsin; Liu, Hsin-Tzu

doi:10.1371/journal.pone.0076779

Cited by 96 publications

(90 citation statements)

References 28 publications

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“…IC patients have high urinary concentrations of immunoglobulin and inflammatory markers, or high serum levels of C‐reactive protein, NGF and pro‐inflammatory cytokines . Bladders with Hunner type IC show diffuse and intense inflammation and overexpression of pro‐inflammatory genes .…”

Section: Pathophysiologymentioning

confidence: 99%

Clinical guidelines for interstitial cystitis and hypersensitive bladder updated in 2015

Ueda²,

et al. 2016

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Clinical guidelines for interstitial cystitis and hypersensitive bladder have been updated as of 2015. The guidelines define interstitial cystitis by the presence of hypersensitive bladder symptoms (discomfort, pressure or pain in the bladder usually associated with urinary frequency and nocturia) and bladder pathology, after excluding other diseases explaining symptoms. Interstitial cystitis is further classified by bladder pathology; either Hunner type interstitial cystitis with Hunner lesions or non-Hunner type interstitial cystitis with mucosal bleeding after distension in the absence of Hunner lesions. Hypersensitive bladder refers to a condition, where hypersensitive bladder symptoms are present, but bladder pathology or other explainable diseases are unproven. Interstitial cystitis and hypersensitive bladder severely affect patients' quality of life as a result of disabling symptoms and/or comorbidities. Reported prevalence suggestive of these disorders varies greatly from 0.01% to >6%. Pathophysiology would be an interaction of multiple factors including urothelial dysfunction, inflammation, neural hyperactivity, exogenous substances and extrabladder disorders. Definite diagnosis of interstitial cystitis and hypersensitive bladder requires cystoscopy with or without hydrodistension. Most of the therapeutic options lack a high level of evidence, leaving a few as recommended therapeutic options.

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Section: Pathophysiologymentioning

confidence: 99%

Clinical guidelines for interstitial cystitis and hypersensitive bladder updated in 2015

Ueda²,

et al. 2016

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“…The upregulated serum tumor necrosis factor-α, IL-1β, IL-6, and IL-8 levels in IC/BPS patients may potentially have a prognostic role and might help physicians choose an appropriate therapeutic agent. One recent study revealed these serum proinflammatory cytokines and chemokine levels were significantly higher in IC/BPS patients than in the controls [71]. Increased expression of these proinflammatory cytokines and chemokine levels in the serum of IC/BPS patients suggests that not only mast cell activation, but also some other inflammatory mediators might play crucial roles in the pathogenesis of IC/BPS.…”

Section: Proteomics Investigation Of the Potential Serum And Urinary mentioning

confidence: 99%

Pathomechanism of Interstitial Cystitis/Bladder Pain Syndrome and Mapping the Heterogeneity of Disease

Jhang

Kuo

2016

Int Neurourol J

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Interstitial cystitis/bladder pain syndrome (IC/BPS) is a heterogeneous syndrome which is usually characterized by urinary frequency, nocturia, and bladder pain. Several pathomechanisms have been proposed, including uroepithelial dysfunction, mast cell activation, neurogenic inflammation, autoimmunity, and occult urinary tract infections. It is possible that an inflammatory process alters regulation of urothelial homeostasis and results in dysfunction of the bladder epithelium. Different phenotypes of IC/BPS have been explored including Hunner and non-Hunner type IC, hypersensitive bladder, and bladder pain both with and without functional somatic syndrome. Different gene expressions have also been found in different IC phenotypes. Abnormal expressions of uroplakin, chondroitin sulfate and adhesive protein E-cadherin, tight junction protein zonula occludens-1 in IC/BPS bladder suggest abnormal epithelial differentiation in this bladder disease. Analysis of inflammatory proteins, or cytokines in the urine or serum provides another diagnostic foundation forIC/BPS subtypes. The involvement of IC/BPS in systemic functional somatic syndrome and other pelvic organ diseases might also subdivide subtypes of IC/BPS. Chronic inflammation, increased urothelial apoptosis, and abnormal urothelial function are closely associated in IC bladders. This article reviews recent research on the pathomechanisms of IC, which might help us in mapping the heterogeneity of the disease.

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“…Multiple independent studies have confirmed that mast cell infiltration is increased in biopsies from IC/PBS patients (Christmas and Rode, 1991; Kastrup et al, 1983; Larsen et al, 2008; Peeker et al, 2000; Spanos et al, 1997; Tomaszewski et al, 2001). These observations have been correlated with increased release of granular contents (Theoharides et al, 1995), elevated nerve growth factor (NGF), histamine, and pro-inflammatory cytokine protein levels in patient serum (Jiang et al, 2013) and urine (Corcoran et al, 2013; Jacobs et al, 2010; Lotz et al, 1994; Yun et al, 1992) samples, and increased density of substance P (SP)-immunopositive nerve fibers and juxtaposition to mast cells in patient biopsies (Pang et al, 1995). Tryptase, a major component of mast cell granules, can bind to and activate protease activated receptor-2 (PAR2) located on adjacent sensory nerve endings (Cenac et al, 2002; Cenac et al, 2007; Sipe et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Urinary bladder hypersensitivity and dysfunction in female mice following early life and adult stress

et al. 2016

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Early adverse events have been shown to increase the incidence of interstitial cystitis/painful bladder syndrome in adulthood. Despite high clinical relevance and reports of stress-related symptom exacerbation, animal models investigating the contribution of early life stress to female urological pain are lacking. We examined the impact of neonatal maternal separation (NMS) on bladder sensitivity and visceral neuroimmune status both prior-to, and following, water avoidance stress (WAS) in adult female mice. The visceromotor response to urinary bladder distension was increased at baseline and 8d post-WAS in NMS mice, while colorectal sensitivity was transiently increased 1d post-WAS only in naïve mice. Bladder micturition rate and output, but not fecal output, were also significantly increased following WAS in NMS mice. Changes in gene expression involved in regulating the stress response system were observed at baseline and following WAS in NMS mice, and WAS reduced serum corticosterone levels. Cytokine and growth factor mRNA levels in the bladder, and to a lesser extent in the colon, were significantly impacted by NMS and WAS. Peripheral mRNA levels of stress-responsive receptors were differentially influenced by early life and adult stress in bladder, but not colon, of naïve and NMS mice. Histological evidence of mast cell degranulation was increased in NMS bladder, while protein levels of protease activated receptor 2 (PAR2) and transient receptor potential ankyrin 1 (TRPA1) were increased by WAS. Together, this study provides new insight into mechanisms contributing to stress associated symptom onset or exacerbation in patients exposed to early life stress.

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Increased Pro-Inflammatory Cytokines, C-Reactive Protein and Nerve Growth Factor Expressions in Serum of Patients with Interstitial Cystitis/Bladder Pain Syndrome

Cited by 96 publications

References 28 publications

Clinical guidelines for interstitial cystitis and hypersensitive bladder updated in 2015

Clinical guidelines for interstitial cystitis and hypersensitive bladder updated in 2015

Pathomechanism of Interstitial Cystitis/Bladder Pain Syndrome and Mapping the Heterogeneity of Disease

Urinary bladder hypersensitivity and dysfunction in female mice following early life and adult stress

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