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Mast cell mediated ion transport in intestine from patients withand without inflammatory bowel disease

机译:肥大细胞介导的肠内离子转运。没有发炎性肠病

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摘要

Background—Mast cells have been shown to regulate intestinal ion transport in animal models and normal human colon but their physiological role in human intestinal inflammatory disorders is unknown.
Aims—To examine mast cell regulation of ion transport in inflammatory bowel disease (IBD).
Subjects and methods—Small and large intestine was obtained from patients with and without IBD undergoing surgical resection. Short circuit current (Isc) responses to rabbit antihuman IgE, histamine, and electrical stimulation were measured in Ussing chambers. Specimens were also examined for mast cell numbers and degree of inflammation.
Results—Isc responses to anti-IgE and histamine were smaller in magnitude in IBD compared with non-IBD tissues. In all tissues, anti-IgE Isc responses were reduced by about 80% in chloride free buffer. The histamine H1 receptor antagonist, pyrilamine, decreased anti-IgE responses in non-IBD tissues. Greater inhibition with pyrilamine was seen in IBD small intestine but its effect was less in IBD colon. Histamine pretreatment of non-IBD control tissues reduced anti-IgE responses to levels seen in IBD colon but had no effect in small intestine. Mast cell numbers were greater in IBD compared with non-IBDsmall intestine while no differences were observed between the colonicgroups. Isc responses to anti-IgE were not correlated withthe degree of mucosal inflammation.
Conclusions—This study provides further evidencethat mast cells are capable of mediating alterations of ion transportin human gut but that this regulatory role may be altered in IBD. Thedata suggest that prior activation of mast cells with release ofhistamine may account for the reduced secretory response to anti-IgEobserved in IBD colonic tissues.

Keywords:mast cells; intestine; ion transport; histamine; ulcerative colitis; Crohn's disease
机译:背景技术在动物模型和正常人类结肠中,肥大细胞已显示出调节肠道离子运输的作用,但它们在人类肠道炎性疾病中的生理作用尚不清楚。
目标-研究炎症性肠病(IBD)中肥大细胞对离子转运的调控。
受试者和方法-大肠和小肠均来自接受或不接受IBD手术切除的患者。在Ussing室中测量了对兔抗人IgE,组胺和电刺激的短路电流(Isc)响应。还检查了标本的肥大细胞数量和炎症程度。
结果-与非IBD组织相比,IBD中Isc对抗IgE和组胺的反应幅度较小。在所有组织中,抗IgE Isc反应在无氯缓冲液中均降低了约80%。组胺H1受体拮抗剂吡咯胺可降低非IBD组织的抗IgE应答。在IBD小肠中发现吡咯胺的抑制作用更大,但在IBD结肠中的作用较小。对非IBD对照组织进行组胺预处理可将抗IgE反应降低至在IBD结肠中观察到的水平,但在小肠中无作用。与非IBD相比,IBD中的肥大细胞数量更多小肠,而结肠之间没有观察到差异组。 Isc对抗IgE的反应与黏膜炎症的程度。
结论-这项研究提供了进一步的证据肥大细胞能够介导离子迁移的改变但在IBD中这种调节作用可能会改变。的数据表明,肥大细胞在激活之前会释放组胺可能是抗IgE分泌反应减少的原因在IBD结肠组织中观察到。

关键字:肥大细胞;肠;离子传输组胺;溃疡性结肠炎;克罗恩病

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