Mast cell activation and response to tolterodine in the rat urinary bladder in a chronic model of intravesical protamine sulfate and bacterial endotoxin-induced cystitis

Choi, Bo-Hwa; Jin, Lin‐Yu; Kim, Khae Hawn; Han, Jee‐Young; Kang, Ju‐Hee; Yoon, Sang Min; Park, Chang‐Shin; Lee, Tack

doi:10.3892/mmr.2014.2262

Cited by 10 publications

(7 citation statements)

References 30 publications

(43 reference statements)

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“…Therefore, IC/BPS patients were usually prescribed antimuscarinic agents, even though guideline for IC/BPS did not include antimuscarinic medication. Interestingly, animal experiments of IC show that antimuscarinic treatment is not effective for detrusor overactivity in a rat model [ 12 ]. Meanwhile, patients who had antimuscarinic treatment showed more severe frequency (14.6 times/d) than patients who did not receive medication (12.7 times/d).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the incidence and risk factors associated with persistent frequency in interstitial cystitis/bladder pain syndrome and the efficacy of antimuscarinic treatment

et al. 2017

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PurposeTo investigate the incidence and risk factors associated with persistent urinary frequency, and to evaluate the efficacy of antimuscarinic treatment.Materials and MethodsInterstitial cystitis/bladder pain syndrome (IC/BPS) patients complaining of persistent urinary frequency despite improved pain were evaluated. Before initial conventional treatment, each patient completed a voiding diary and symptom questionnaires. After conventional treatment, patients were divided according to the presence of pain and frequency. Improved pain was defined as lesser than 3 points in visual analogue scale, and persistent urinary frequency as >10 times/d. Risk factors for persistent frequency were identified through multivariate analysis. The efficacy of antimuscarinic treatment was assessed by the mean change of frequency.ResultsOf 171 IC/BPS patients treated with conventional therapy, 132 had improved pain after 3 months, but 72 had persistent frequency (72 of 132, 54.5%). Patients with persistent frequency had lower voided volume (p=0.008), lower maximal flow rate (p<0.001), lower maximal bladder capacity (p=0.003), and more frequent micturition (p<0.001) at baseline compared to those with improved frequency. Patients who took antimuscarinic agents showed slightly decreased urinary frequency, from 14.6 times/d to 13.5 times/d (p=0.438) after 3 months of medication. No patients showed more than a 20% decrease in frequency with antimuscarinics.ConclusionsAbout half of the patients with IC/BPS showed persistent frequency, with poor voiding function identified as a risk factor; antimuscarinic treatment was not effective in these patients.

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Section: Discussionmentioning

confidence: 99%

Evaluation of the incidence and risk factors associated with persistent frequency in interstitial cystitis/bladder pain syndrome and the efficacy of antimuscarinic treatment

et al. 2017

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“…PS treatment destroys the bladder glycosaminoglycan (GAGs) layer, leading to enhancement of the LPS action. Animal models including ours bear 3 similarities to currently known pathophysiologic steps of human IC 4,28 At first, PS damaged the bladder mucus, and then urothelium was injured by bacterial toxins such as LPS. 4 Following these steps, the injured mucus and urothelium are exposed to rat's urine for an additional one month to give enough time for inducing chronic inflammation into the injured bladder wall by the toxins from urine.…”

Section: Introductionmentioning

confidence: 87%

“…Animal models including ours bear 3 similarities to currently known pathophysiologic steps of human IC 4,28 At first, PS damaged the bladder mucus, and then urothelium was injured by bacterial toxins such as LPS. 4 Following these steps, the injured mucus and urothelium are exposed to rat's urine for an additional one month to give enough time for inducing chronic inflammation into the injured bladder wall by the toxins from urine. Our previous findings in this rat model demonstrated the involvement of degranulated mast cells, which was consistent with observation in the human bladder affected with IC.…”

Section: Introductionmentioning

confidence: 87%

“…Our previous findings in this rat model demonstrated the involvement of degranulated mast cells, which was consistent with observation in the human bladder affected with IC. Over 50% of patients have mast cells in lamina propria 4,26 Mast cells have been considered to play key pathophysiological roles in the initiation and propagation of inflammation, by the production proinflammatory mediators, neurotrophic factors and immunoregulatory cytokines. 25 Mast cells also secrete nerve growth factor (NGF) leading to the neuropathic pain, one of IC characteristics.…”

Section: Introductionmentioning

confidence: 99%

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Differential perturbation of the interstitial cystitis-associated genes of bladder and urethra in rat model

et al. 2017

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Interstitial cystitis (IC) is a chronic bladder dysfunction characterized as urinary frequency, urgency, nocturia, and pelvic pain. The changes in urethra may wind up with the bladder changes in structure and functions, however, the functions of the urethra in IC remains elusive. The aim of this study was to understand the perturbed gene expression in urethra, compared with urinary bladder, associated with the defected urodynamics. Using female IC mimic rats, a comprehensive RNA-sequencing combined with a bioinformatics analysis was performed and revealed that IC-specific genes in bladder or urethra. Gene ontology analysis suggested that the cell adhesion or extracellular matrix regulation, intracellular signaling cascade, cardiac muscle tissue development, and second messenger-mediated signaling might be the most enriched cellular processes in IC context. Further study of the effects of these bladder- or urethra-specific genes may suggest underlying mechanism of lower urinary tract function and novel therapeutic strategies against IC.

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“…Mast cells play an important role in responding to increased alarmin levels released from damaged epithelial cells [ 58 ]. In a rat model of IC, there was significantly more mast cell infiltration compared to that seen in control rats, and most of the cells were degranulated [ 85 ].…”

Section: Implications For Clinical Urologymentioning

confidence: 99%

Interleukin-33 and Mast Cells Bridge Innate and Adaptive Immunity: From the Allergologist’s Perspective

Jang¹,

Kim²

2015

Int Neurourol J

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Interleukin (IL) 33, a member of the IL-1 superfamily, is an “alarmin” protein and is secreted in its active form from damaged cells undergoing necrotic cell death. Mast cells are one of the main effector cell types in allergic disorders. They secrete a variety of mediators, including T helper 2 cytokines. As mast cells have high-affinity IgE receptors (FcεRI) on their surface, they can capture circulating IgE. IgE-bound mast cells degranulate large amounts of histamine, heparin, and proteases when they encounter antigens. As IL-33 is an important mediator of innate immunity and mast cells play an important role in adaptive immune responses, interactions between the two could link innate and adaptive immunity. IL-33 promotes the adhesion of mast cells to laminin, fibronectin, and vitronectin. IL-33 increases the expression of adhesion molecules, such as intracellular adhesion molecule-1 and vascular cell adhesion molecule-1, in endothelial cells, thus enhancing mast cell adhesion to blood vessel walls. IL-33 stimulates mast cell proliferation by activating the ST2/Myd88 pathway; increases mast cell survival by the activation of survival proteins such as Bcl-XL; and promotes the growth, development, and maturation of mast cell progenitors. IL-33 is also involved in the activation of mature mast cells and production of different proinflammatory cytokines. The interaction of IL-33 and mast cells could have important clinical implications in the field of clinical urology. Epithelial dysfunction and mast cells could play an important role in the pathogenesis of interstitial cystitis. Urinary levels of IL-33 significantly increase in patients with interstitial cystitis. In addition, the number of mast cells significantly increase in the urinary bladders of patients with interstitial cystitis. Therefore, inhibition of mast cell activation and degranulation in response to increase in IL-33 is a potential therapeutic target in the treatment of interstitial cystitis.

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Mast cell activation and response to tolterodine in the rat urinary bladder in a chronic model of intravesical protamine sulfate and bacterial endotoxin-induced cystitis

Cited by 10 publications

References 30 publications

Evaluation of the incidence and risk factors associated with persistent frequency in interstitial cystitis/bladder pain syndrome and the efficacy of antimuscarinic treatment

Evaluation of the incidence and risk factors associated with persistent frequency in interstitial cystitis/bladder pain syndrome and the efficacy of antimuscarinic treatment

Differential perturbation of the interstitial cystitis-associated genes of bladder and urethra in rat model

Interleukin-33 and Mast Cells Bridge Innate and Adaptive Immunity: From the Allergologist’s Perspective

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