O'Sullivan M, Clayton N, Breslin N P, Harman I, Bountra C, McLaren A, O'Morain C A
Adelaide & Meath Hospitals, Trinity College Dublin, Ireland.
Neurogastroenterol Motil. 2000 Oct;12(5):449-57. doi: 10.1046/j.1365-2982.2000.00221.x.
Mast cells (MC) release potent mediators which alter enteric nerve and smooth muscle function and may play a role in the pathogenesis of the irritable bowel syndrome (IBS). The aim of this study was to determine if MC were increased in the colon of IBS patients compared to controls. Biopsy specimens were obtained from the caecum, ascending colon, descending colon and rectum of 28 patients: 14 IBS (Rome criteria); seven normal; and seven inflammatory controls. Tissue was stained immunohistochemically using a monoclonal mouse antibody for human mast cell tryptase (AA1). Tissue area occupied by tryptase-positive MC (volume density of mast cells) was quantified by image analysis. The number of plasma cells, lymphocytes, eosinophils, neutrophils and macrophages were each graded semiquantitatively (0-4) in haematoxylin and eosin stained sections. Mast cell volume density was significantly (P < 0.05) higher in IBS (0.91 +/- 0.18; CI 0.79; 1.0) than normal controls (0.55 +/- 0.14; CI 0.40; 0.69) in the caecum but not at other sites. Apart from MC, there was no evidence of increased cellular infiltrate in the IBS group. MC were significantly increased in the caecum of IBS patients compared to controls. The multiple effects of the intestinal mast cell alone, or as a participant of a persistent inflammatory response, may be fundamental to the pathogenesis of IBS.
肥大细胞(MC)释放强效介质,这些介质可改变肠神经和平滑肌功能,并可能在肠易激综合征(IBS)的发病机制中起作用。本研究的目的是确定与对照组相比,IBS患者结肠中的MC是否增多。从28例患者的盲肠、升结肠、降结肠和直肠获取活检标本:14例IBS患者(符合罗马标准);7例正常人;7例炎症对照。使用抗人肥大细胞类胰蛋白酶的单克隆小鼠抗体(AA1)对组织进行免疫组织化学染色。通过图像分析对类胰蛋白酶阳性MC所占的组织面积(肥大细胞体积密度)进行定量。在苏木精和伊红染色切片中,对浆细胞、淋巴细胞、嗜酸性粒细胞、中性粒细胞和巨噬细胞的数量分别进行半定量分级(0-4级)。IBS患者盲肠中的肥大细胞体积密度(0.91±0.18;可信区间0.79;1.0)显著高于正常对照组(0.55±0.14;可信区间0.40;0.69)(P<0.05),但在其他部位无此差异。除MC外,IBS组没有细胞浸润增加的证据。与对照组相比,IBS患者盲肠中的MC显著增多。肠道肥大细胞单独的多种作用,或作为持续性炎症反应的参与者,可能是IBS发病机制的基础。