Patrick M K, Dunn I J, Buret A, Miller H R, Huntley J F, Gibson S, Gall D G
Intestinal Disease Research Unit, University of Calgary, Alberta, Canada.
Gastroenterology. 1988 Jan;94(1):1-9. doi: 10.1016/0016-5085(88)90603-8.
Intestinal anaphylaxis is associated with disturbances in gut function that are antigen-specific and dependent on mast cell degranulation. Using an animal model of intestinal anaphylaxis, we have correlated alterations in water and electrolyte transport, associated with intraluminal challenge, with specific intestinal mucosal mast cell degranulation by following systemic as well as local release of rat mast cell protease II. This protease is specific for intestinal mucosal mast cells and is known to selectively attack type IV collagen, which is found in basement membranes. Intraluminal antigen challenge in sensitized animals dramatically increased serum and intraluminal levels of rat mast cell protease II. Serum levels continued to rise throughout the duration of antigen challenge. Although light microscopy of challenged intestine demonstrated little distortion of mucosal architecture, ultrastructural examination revealed significant disruption to the basement membrane and underlying collagenous matrix of the intestinal mucosa. Our findings indicate that during mucosal immunoglobulin E-mediated reactions, rat mast cell protease II is released and is associated with ultrastructural changes in the intestinal mucosa. The systemic appearance of this specific protease provides a serum marker of intestinal anaphylaxis.
肠道过敏反应与肠道功能紊乱有关,这种紊乱是抗原特异性的,且依赖于肥大细胞脱颗粒。利用肠道过敏反应的动物模型,我们通过追踪大鼠肥大细胞蛋白酶II的全身及局部释放情况,将腔内刺激引起的水和电解质转运变化与特定的肠道黏膜肥大细胞脱颗粒联系起来。这种蛋白酶对肠道黏膜肥大细胞具有特异性,已知它能选择性地攻击基底膜中发现的IV型胶原。致敏动物的腔内抗原刺激显著增加了大鼠肥大细胞蛋白酶II的血清和腔内水平。在抗原刺激期间,血清水平持续上升。尽管对受刺激肠道的光学显微镜检查显示黏膜结构几乎没有变形,但超微结构检查揭示了肠道黏膜基底膜和下方胶原基质的显著破坏。我们的研究结果表明,在黏膜免疫球蛋白E介导的反应过程中,大鼠肥大细胞蛋白酶II被释放,并与肠道黏膜的超微结构变化有关。这种特异性蛋白酶的全身出现为肠道过敏反应提供了一种血清标志物。