INTERSTITIAL CYSTITIS - BLADDER MUCOSA LYMPHOCYTE IMMUNOPHENOTYPING AND PERIPHERAL-BLOOD FLOW-CYTOMETRY ANALYSIS
INTERSTITIAL CYSTITIS - BLADDER MUCOSA LYMPHOCYTE IMMUNOPHENOTYPING AND PERIPHERAL-BLOOD FLOW-CYTOMETRY ANALYSIS
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DOI：
10.1016/s0022-5347(17)39611-8
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发表时间：
1990-10-01
影响因子：
6.6
通讯作者：
JOHANSSON, SL
中科院分区：
文献类型：
--
作者：
HARRINGTON, DS;FALL, M;JOHANSSON, SL
间质性膀胱炎是一种病因不明的慢性膀胱疾病，主要发生在女性身上，以急症和疼痛为特征。虽然免疫机制与疾病过程有关，但对局部或外周血免疫反应知之甚少。通过经尿道膀胱切除术获得的43例（24例为典型膀胱炎，9例为非溃疡性或早期间质性膀胱炎，10例为对照）快速冷冻膀胱活检切片，采用单克隆抗体和亲和素-生物素免疫过氧化物酶技术分析膀胱粘膜局部免疫反应。同时，用流式细胞术分析24例患者（9例经典和5例非溃疡性早期间质性膀胱炎，10例对照组）的肝素化外周血（10 cc），使用相同的抗体。对照组活检（中位年龄44岁，范围27 - 52岁）无溃疡，淋巴样细胞（主要是T辅助细胞）较少，罕见的T细胞结节，无B细胞。非溃疡组（中位年龄39岁，范围29至44岁）有罕见的粘膜破裂，但没有溃疡，淋巴样细胞轻微增加（主要是T辅助细胞），偶尔有T细胞聚集，没有B细胞结节和罕见的浆细胞。对照组与非核性间质性膀胱炎患者间无统计学差异。相比之下，经典间质性膀胱炎组（中位年龄68岁，范围47 - 73岁）有溃疡，伴浆细胞局灶性炎症，T细胞聚集，B细胞结节包括生发中心，辅助细胞与抑制细胞的比例降低或正常，生发中心有抑制细胞毒性细胞。外周血淋巴细胞亚群的流式细胞术分析显示，对照组正常，非溃疡组分泌Ig阳性B细胞和活化淋巴细胞数量增加，经典组分泌Ig阳性B细胞和活化淋巴细胞数量增加，kappa- λ比轻度异常。我们认为免疫机制至少在间质性膀胱炎的病理生理中起部分作用。间质性膀胱炎与炎症性肠病有明显的相似之处。建议进行进一步的研究。
Interstitial cystitis is a chronic bladder disorder of unknown etiology that primarily afflicts women and is characterized by urgency and pain. Although immune mechanisms have been implicated in the disease process, little is known about the local or peripheral blood immune responses. Cryostat sections of snap-frozen bladder biopsies obtained by transurethral resection from 43 patients (24 with classical and 9 with nonulcerative or early interstitial cystitis, and 10 controls) were analyzed using a panel of monoclonal antibodies with an avidin-biotin immunoperoxidase technique to characterize the local immune response of bladder mucosa. Simultaneously obtained heparinized peripheral blood (10 cc) was analyzed by flow cytometry in 24 patients (9 with classical and 5 with nonulcerative early interstitial cystitis, and 10 controls) using the same panel of antibodies. The control group biopsies (median age 44 years, range 27 to 52 years) had no ulcers, few lymphoid cells (predominately T-helper cells), rare T cell nodules and no B cells. The nonulcer group (median age 39 years, range 29 to 44 years) had rare mucosal ruptures but no ulcers, slightly increased lymphoid cells (predominately T-helper), occasional T cell aggregates, no B cell nodules and rare plasma cells. No statistically significant difference between control and nonuclerative interstitial cystitis patients was identified. In contrast, the classical interstitial cystitis group (median age 68 years, range 47 to 73 years) had ulcers, intense inflammation with focal sheets of plasma cells, aggregates of T cells, B cell nodules including germinal centers, a decreased or normal helper-to-suppressor cell ratio and suppressor cytotoxic cells in germinal centers. Flow cytometry analysis of peripheral blood lymphocyte subsets showed normal patterns in controls, increased numbers of secretory Ig positive B cells and activated lymphocytes in the nonulcerative group, and increased numbers of secretory Ig positive B cells with mildly abnormal kappa-to-lambda ratios and activated lymphocytes in the classical group. We conclude that an immune mechanism has at least a partial role in the pathophysiology of interstitial cystitis. A parallel between interstitial cystitis and inflammatory bowel disease is evident. Further studies are indicated.