摘要

背景:克罗恩病和溃疡性结肠炎是特发性炎症性肠病(IBD)，涉及花生四烯酸(AA)通过磷脂酶A2 (PLA2)从膜磷脂中释放，合成类烯二糖。一个潜在的重要调节这些介质的生产是PLA2的蛋白质激活物，称为PLA2激活蛋白(PLAP)。目的:探讨炎症性肠病患者炎症肠组织和结肠炎小鼠肠组织中PLAP值是否可能升高。患者:接受诊断性肠镜检查的溃疡性结肠炎和克罗恩病患者的活检标本，手术切除无IBD的患者的结肠黏膜均为正常。方法:采用免疫细胞化学方法，用PLAP合成肽的亲和纯化抗体对IBD患者的肠活检标本切片与正常肠组织切片进行PLAP抗原定位。用小鼠[32P]标记的plap cDNA探针对小鼠结肠中提取的RNA进行了Northern blot分析，这些RNA来自于喂食葡聚糖硫酸钠(DSS)的小鼠和暴露于脂多糖(LPS)的培养HT-29细胞。结果:在IBD患者的肠组织切片中，PLAP抗原主要定位于单核细胞和粒细胞内，细胞外PLAP抗原的额外沉积与血管和炎症组织中的水肿液有关。相比之下，正常人肠组织切片除肠腔上皮细胞有较弱的细胞质反应外，无PLAP反应抗原。与对照组相比，DSS处理的小鼠结肠组织中PLAP抗原的含量也有所增加。DSS处理小鼠结肠黏膜固有层基质与PLAP合成肽的抗体发生强烈反应，而对照组小鼠结肠未观察到任何反应。 These data were supported by northern analysis which showed that PLAP mRNA was increased in the colons of DSS treated mice and cultured HT-29 cells exposed to LPS. CONCLUSIONS: As PLAP values were increased in the intestinal mucosa of IBD patients and mice with colitis, as well as in LPS treated cultured HT-29 cells, a role was postulated for PLAP in increasing PLA2 activity, which leads to the increased synthesis of eicosanoids in intestinal tissues of patients with these inflammatory diseases.