Stenson W F
Division of Gastroenterology, Jewish Hospital, St. Louis, Missouri 63110.
Scand J Gastroenterol Suppl. 1990;172:13-8. doi: 10.3109/00365529009091903.
An unknown initiating event in inflammatory bowel disease (IBD) activates the immune system, which is followed by infiltration of the intestinal mucosa with inflammatory cells and the production of soluble mediators of inflammation. These mediators of inflammation include the metabolites of arachidonic acid. The results of research on arachidonic acid metabolites are reviewed, and it is concluded that the major arachidonic metabolites in human IBD mucosa are the lipoxygenase products leukotriene B4 (LTB4) and 5-hydroxy-6,8,11,14-eicosatetraenoic acid. These metabolites are found in much higher concentrations in mucosa from patients with IBD than from healthy controls. Significantly more chemotactic activity is found in IBD mucosa than in healthy mucosa, and most of this activity is attributable to LTB4. Enhanced synthesis of LTB4 could account for much of the inflammatory response in IBD. Inhibition of the lipoxygenase pathway could be the mechanism that accounts for the therapeutic efficacy of mesalazine.
炎症性肠病（IBD）中一个未知的起始事件激活了免疫系统，随后炎症细胞浸润肠黏膜并产生可溶性炎症介质。这些炎症介质包括花生四烯酸的代谢产物。本文综述了关于花生四烯酸代谢产物的研究结果，并得出结论：人类IBD黏膜中的主要花生四烯酸代谢产物是脂氧合酶产物白三烯B4（LTB4）和5-羟基-6,8,11,14-二十碳四烯酸。与健康对照相比，这些代谢产物在IBD患者的黏膜中浓度要高得多。IBD黏膜中的趋化活性明显高于健康黏膜，且大部分这种活性归因于LTB4。LTB4合成增强可能是IBD中大部分炎症反应的原因。抑制脂氧合酶途径可能是美沙拉嗪治疗效果的作用机制。
