Perdue M H, Marshall J, Masson S
Department of Pathology, McMaster University, Hamilton, Ontario, Canada.
Gastroenterology. 1990 Mar;98(3):561-7. doi: 10.1016/0016-5085(90)90274-5.
Basal and stimulated changes in ion transport in vitro were examined in jejunal mucosa from rats during inflammation produced after infection with the nematode Nippostrongylus brasiliensis. The gut was acutely inflamed at days 7 and 10 when net secretion of Na+ and Cl- ions was evident. Serum levels of rat mast cell protease II were elevated, providing evidence for mast cell activation. In addition, the magnitude of the short-circuit current responses to electrical transmural stimulation of enteric nerves (but not to histamine in the presence of neural blockade) were significantly reduced (p less than 0.01) to 17%-33% of control values, suggesting abnormalities of mucosal nerves. Following worm expulsion, serum levels of rat mast cell protease II and ion transport returned to normal. However, mastocytosis was apparent in gut mucosa and parasite antigen stimulated net secretion. In the absence of antigen, short-circuit current responses to nerve stimulation were increased (to 122% of controls; p less than 0.05). These findings suggest that changes in mast cells and enteric nerves occur during inflammation in this model and implicate neural and mast cell interactions with the epithelium in producing the ion-transport abnormalities.
在感染巴西日圆线虫后引发炎症的大鼠空肠黏膜中，检测了体外离子转运的基础变化和刺激变化。在第7天和第10天肠道出现急性炎症，此时Na⁺和Cl⁻离子的净分泌明显。大鼠肥大细胞蛋白酶II的血清水平升高，为肥大细胞活化提供了证据。此外，对肠神经进行电透壁刺激（但在存在神经阻滞的情况下对组胺无反应）所产生的短路电流反应幅度显著降低（p<0.01），降至对照值的17%-33%，提示黏膜神经存在异常。蠕虫排出后，大鼠肥大细胞蛋白酶II的血清水平和离子转运恢复正常。然而，肠道黏膜中肥大细胞增多明显，且寄生虫抗原刺激净分泌。在无抗原的情况下，对神经刺激的短路电流反应增加（达到对照值的122%；p<0.05）。这些发现表明，在该模型的炎症过程中肥大细胞和肠神经发生了变化，提示神经和肥大细胞与上皮细胞的相互作用导致了离子转运异常。
