Mucosal proinflammatory cytokine production correlates with endoscopic activity of ulcerative colitis
Mucosal proinflammatory cytokine production correlates with endoscopic activity of ulcerative colitis
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DOI：
10.1007/s005350050218
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发表时间：
1999-02-01
影响因子：
6.3
通讯作者：
Ishiguro, Y
中科院分区：
文献类型：
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作者：
Ishiguro, Y
促炎细胞因子被认为参与溃疡性结肠炎（UC）的发病机制。本研究的目的是阐明UC患者在疾病难治性、内镜检查结果和宿主对脂多糖（LPS）刺激的反应方面促炎细胞因子产生的概况。结肠粘膜组织来自活动性UC患者（n = 15，包括4例难治性疾病患者）和非活动性UC患者（n = 7）、非炎性肠病（IBD）结肠炎患者（n = 11）和对照组（n = 20）。进行器官培养，并通过酶联免疫吸附测定（ELISA）测定培养基中四种细胞因子（下文描述）的量。LPS刺激增强白细胞介素（IL）-1 β。IL-8和IL-6的产生，但仅在活动性UC标本中增强肿瘤坏死因子（TNF）-α的产生。活动性UC患者的IL-6、IL-8和TNF-α水平显著高于非IBD结肠炎患者。并且所有这三种细胞因子的产生与内窥镜检查的炎症等级相关。这些细胞因子的产生也显着较高的难治性疾病患者接受皮质类固醇比非难治性疾病患者接受皮质类固醇。这些结果表明，粘膜促炎细胞因子的产生增加可能与UC的发病机制有关。
Proinflammatory cytokines are believed to be involved in the pathogenesis of ulcerative colitis (UC). The aim of this study was to clarify the profiles of proinflammatory cytokine production in patients with UC in terms of disease intractability, endoscopic findings, and host response to lipopolysaccharide (LPS) stimulation. Colonic mucosal tissues were obtained from patients with active UC (n = 15, including 4 patients with intractable disease) and inactive UC (n = 7), non-inflammatory bowel disease (IBD) colitis (n = 11), and controls (n = 20). Organ culture was performed, and the amounts of four cytokines (described below in the culture media were determined by enzyme-linked immunosorbent assay (ELISA). LPS stimulation enhanced interleukin (IL)-1 beta. IL-8, and IL-6 production in colonic specimens from all groups, but enhanced tumor necrosis factor (TNF)-alpha production only in active UC specimens. Levels of IL-6, IL-8, and TNF-alpha were significantly higher in active UC than in non-IBD colitis. and the production of all three of these cytokines was correlated to the endoscopic grade of inflammation. The production of these cytokines was also significantly higher in patients with intractable disease receiving corticosteroids than in patients with non-intractable disease receiving corticosteroids. These results suggest that enhanced production of mucosal proinflammatory cytokines may be implicated in the pathogenesis of UC.