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炎症性肠病患者肠道单核细胞和上皮细胞中的(2'-5')寡腺苷酸合成酶活性

(2'-5')Oligoadenylate synthetase activity in intestinal mononuclear and epithelial cells of inflammatory bowel disease patients.

作者信息

Rachmilewitz D, Stalnikowicz R, Karmeli F, Youngman K, Fiocchi C

机构信息

Dept. of Gastroenterology, Hadassah University Hospital, Hebrew University-Hadassah Medical School, Jerusalem, Israel.

出版信息

Scand J Gastroenterol. 1988 Oct;23(8):941-7. doi: 10.3109/00365528809090151.

DOI:10.3109/00365528809090151
PMID:3201131
Abstract

The activity of (2'-5')oligoadenylate synthetase, an enzyme induced by and mediating the antiviral action of interferon, was measured in extracts of intestinal mononuclear and epithelial cells isolated from patients with Crohn's disease, ulcerative colitis, and a control group. No significant differences were detected among (2'-5')oligoadenylate synthetase activities of lamina propria mononuclear cells derived from inflammatory bowel disease-involved and histologically normal control mucosa. Similarly, epithelial cells from inflammatory bowel disease and control patients expressed comparable levels of the enzyme, but these were significantly higher (p less than 0.01) than those found in autologous mononuclear cells. These results indicate that interferon is locally produced along the human intestinal mucosa under normal and inflammatory conditions. While this study supports the contention that induction of an antiviral state does not play a significant role in the pathogenesis of inflammatory bowel disease, it does not exclude the activation of the interferon system for other immunologic functions.

摘要

(2'-5')寡腺苷酸合成酶是一种由干扰素诱导并介导其抗病毒作用的酶,对从克罗恩病、溃疡性结肠炎患者及对照组分离出的肠道单核细胞和上皮细胞提取物中的该酶活性进行了测定。炎症性肠病累及的黏膜固有层单核细胞与组织学正常的对照黏膜的(2'-5')寡腺苷酸合成酶活性之间未检测到显著差异。同样,炎症性肠病患者和对照患者的上皮细胞表达的该酶水平相当,但显著高于自体单核细胞中的水平(p<0.01)。这些结果表明,在正常和炎症条件下,干扰素在人肠道黏膜中局部产生。虽然本研究支持抗病毒状态的诱导在炎症性肠病发病机制中不发挥重要作用这一观点,但并不排除干扰素系统因其他免疫功能而被激活。

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引用本文的文献

1
Production of inflammatory cytokines in the intestinal lamina propria.肠道固有层中炎性细胞因子的产生。
Immunol Res. 1991;10(3-4):239-46. doi: 10.1007/BF02919699.