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Lewis大鼠实验性自身免疫性膀胱炎:间质性膀胱炎的一种潜在动物模型。

Experimental autoimmune cystitis in the Lewis rat: a potential animal model for interstitial cystitis.

作者信息

Luber-Narod J, Austin-Ritchie T, Banner B, Hollins C, Maramag C, Price H, Menon M

机构信息

Department of Surgery, University of Massachusetts Medical School, Worcester 01655, USA.

出版信息

Urol Res. 1996;24(6):367-73. doi: 10.1007/BF00389795.

DOI:10.1007/BF00389795
PMID:9008331
Abstract

To develop an autoimmune animal model for interstitial cystitis (IC), we injected rats with Freund's adjuvant (CFA) containing bladder homogenate (experimentals) or CFA alone (shams). We observed a doubling of urinary frequency in the experimental animals over the shams (P = 0.004) and histopathologic changes (venular congestion) consistent with IC. Statistically significant bladder capacity changes were not found. Mast cell (MC) number was not statistically different between experimentals and controls but the number of MCs from section to adjacent section within the same animal's bladder did vary markedly, indicating the MC counts are not a reliable measure of disease in the rat bladder. Splenocytes cultured from the experimental animals and transferred to naive syngeneic recipients were capable of transferring the urinary frequency changes and vascular congestion while splenocytes from animals which did not develop the condition were without effect. In summary, we have developed and autoimmune model for IC consistent with the clinical features of IC. The features of this model can be transferred to naive syngeneic recipients via adoptive splenocyte transfer. The model will permit us to ask and answer important questions about the pathogenesis and treatment of the human disease.

摘要

为了建立间质性膀胱炎(IC)的自身免疫动物模型,我们给大鼠注射含有膀胱匀浆的弗氏完全佐剂(CFA)(实验组)或仅注射CFA(假手术组)。我们观察到,与假手术组相比,实验组动物的排尿频率增加了一倍(P = 0.004),并且出现了与IC一致的组织病理学变化(小静脉充血)。未发现膀胱容量有统计学意义的变化。实验组和对照组之间肥大细胞(MC)数量无统计学差异,但同一动物膀胱内不同切片间的MC数量变化显著,这表明MC计数不是大鼠膀胱疾病的可靠指标。从实验组动物分离培养并转移至同基因未致敏受体的脾细胞能够传递排尿频率变化和血管充血情况,而未发生该病症的动物的脾细胞则无此作用。总之,我们建立了一个与IC临床特征相符的IC自身免疫模型。该模型的特征可通过脾细胞过继转移传递给同基因未致敏受体。该模型将使我们能够提出并回答有关人类疾病发病机制和治疗的重要问题。

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Uroplakin peptide-specific autoimmunity initiates interstitial cystitis/painful bladder syndrome in mice.尿路上皮肽特异性自身免疫反应引发小鼠间质性膀胱炎/膀胱疼痛综合征。
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Urothelial antigen-specific CD4+ T cells function as direct effector cells and induce bladder autoimmune inflammation independent of CD8+ T cells.尿路上皮抗原特异性 CD4+ T 细胞作为直接效应细胞,在不依赖 CD8+ T 细胞的情况下诱导膀胱自身免疫炎症。
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Intravesical dimethyl sulfoxide inhibits acute and chronic bladder inflammation in transgenic experimental autoimmune cystitis models.膀胱内注射二甲基亚砜可抑制转基因实验性自身免疫性膀胱炎模型中的急性和慢性膀胱炎症。
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