Symptoms of Bladder Pain Syndrome

Warren, John W.; Hanno, Philip M.

doi:10.1007/978-1-4419-6929-3_12

Cited by 1 publication

(1 citation statement)

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“…In addition, CFAinjected WT mice had significantly lower 50% response thresholds than CFA-injected Ccr2 uroplakin 2 protein induced a proinflammatory type 1 cytokine response in the bladder and increased urinary frequency but without detectable tactile allodynia (4). In the present study, we focused on the allodynia phenotype in the UPK3A 65-84 model, because it is considered the most distressing symptom of IC/PBS (55). By assessing tactile allodynia at multiple time points, we showed that our EAC mice develop early and chronic pain-like behavior in the pelvic (suprapubic) and hindpaw regions.…”

Section: Discussionmentioning

confidence: 96%

Chronic pelvic allodynia is mediated by CCL2 through mast cells in an experimental autoimmune cystitis model

Bicer

Altuntas

İzgi

et al. 2015

American Journal of Physiology-Renal Physiology

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The cause of chronic pelvic pain in interstitial cystitis/painful bladder syndrome (IC/PBS) remains unclear; autoimmunity is a possible etiology. We have recently shown that injection of a single immunogenic peptide of uroplakin 3A (UPK3A 65-84) induces experimental autoimmune cystitis (EAC) in female BALB/cJ mice that is unique among experimental models in accurately reflecting both the urinary symptoms and pelvic pain of IC/PBS. The aim of this project was to identify the roles of mast cells and mast cell chemoattractant/activator monocyte chemoattractant protein-1 [chemokine (C-C motif) ligand 2 (CCL2)] in the allodynia in this model. We immunized 6- to 8-wk-old female BALB/cJ mice with UPK3A 65-84 peptide and, 5–40 days later, observed increased responses to stimulation of the suprapubic abdominal and hindpaw surfaces with von Frey monofilaments compared with mice injected with adjuvant alone. Suprapubic and hindpaw tactile allodynia responses by EAC mice were blocked by instillation of lidocaine into the bladder but not by lidocaine in the uterus, confirming the bladder as the source of the hypersensitivity. Markedly increased numbers of activated mast cells and expression of CCL2 were found in the bladder after immunization with UPK3A 65-84. Hypersensitive responses were inhibited by mast cell stabilizer cromolyn sodium and antagonists of histamine receptors 1 and 2. Furthermore, BALB/cJ mice with deletion of the Ccl2 or chemokine (C-C motif) receptor 2 gene exhibited markedly reduced allodynia and accumulation of mast cells after UPK3A 65-84 immunization. These results show that UPK3A 65-84 immunization causes chronic visceral allodynia and suggest that it is mediated by CCL2-driven mast cell accumulation in the bladder.

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Section: Discussionmentioning

confidence: 96%