Objective. Interstitial cystitis/bladder pain syndrome (IC/BPS) is characterized by overexpression of monocyte chemoattractant protein-1 (MCP-1) in bladder tissues and induction of mast cell (MC) degranulation. This study was undertaken to explore the mechanism of action of MCP-1 in the development of IC/BPS. Methods. A rat model of IC/BPS was developed by perfusing bladders of nine SPF- grade female Sprague-Dawley rats with protamine sulfate and lipopolysaccharide (PS+LPS). MCP-1 and histamine levels in bladder tissue and urine were detected by immunohistochemistry and ELISA. MC degranulation was measured by immunofluorescence techniques and chemokine (C-C motif) receptor 2 (CCR2) was assayed by flow cytometry. Results. Increased MCP-1 expression in bladder tissue and elevated MCP-1 and histamine levels were observed in the urine of LS+LPS-treated rats. This was accompanied by the expression of CCR2 on MC surfaces, suggesting MCP-1 may induce MC degranulation through CCR2. Exposure to LPS stimulated MCP-1 expression in bladder epithelial cells, and exposure to MCP-1 induced histamine release from MCs. Conclusions. MCP-1 upregulation in IC/BPS is one of possible contributing factors inducing histamine release from MCs. CCR2 is involved in the process of mast cell degranulation in bladder tissues. These changes may contribute to the development of symptoms of IC/BPS. 1. Introduction Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic inflammatory condition that is difficult to characterize without precise knowledge of the symptoms and histology that characterizes the disease [1]. Commonly observed symptoms include urinary frequency, urgency, and suprapublic pain that often drastically affect the quality of life of affected patients [2–4]. It is generally thought that the development and progression of IC/BPS is associated with infection, defects in bladder permeability, immune or neuroendocrine disorders, and genetic disorders related to visceral hypersensitivity [5–7]. Despite comprehensive characterization of symptoms and histology of IC/BPS in recent decades, its exact etiology remains unclear, limiting the development of effective therapeutic interventions. Mast cells (MCs), long suspected to play a role in the onset of IC/BPS, are derived from specific precursors localized in the bone marrow [8]. These precursors are stimulated to maturation by local tissue microenvironmental factors that vary according to the tissue types [9]. MC stimulation has been shown to facilitate the degranulation and release of vasoactive, proinflammatory, and
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