Scudamore C L, Pennington A M, Thornton E, McMillan L, Newlands G F, Miller H R
Department of Veterinary Clinical Studies, Veterinary Field Station, Easter Bush, Roslin, Midlothian.
Gut. 1995 Aug;37(2):235-41. doi: 10.1136/gut.37.2.235.
The kinetics of the release of rat mast cell protease-II (RMCP-II) from mucosal mast cells in the jejunum of Nippostrongylus brasiliensis primed (immune) rats was investigated using ex vivo perfusion of a segment of jejunum through the cranial mesenteric artery. The aim of the study was to assess the role of the protease in anaphylaxis and in particular to ascertain whether it is responsible for the histological changes, which include widespread epithelial shedding, seen in the mucosa in in vivo models of anaphylaxis. Perfusion of the jejunal vasculature with a Krebs-Ringer buffer showed that there was basal secretion of RMCP-II by jejunal mast cells in all rats studied. The baseline concentration of RMCP-II was significantly greater (p < 0.05) in immune rats (> 7 ng/ml) previously exposed to nippostrongylus infection than in control, naive animals (< 2 ng/ml). Challenge of immune rats with 100 or 400 worm equivalents of whole worm antigen resulted in an immediate (within 40 seconds) and significant (p < 0.02) increase in the concentration of RMCP-II (to > 3 micrograms/ml) in the vascular perfusate, which was not seen in naive rats or immune rats challenged with an irrelevant antigen. Greater amounts of RMCP-II were also recovered from the jejunal lumen of immune rats compared with naive rats after challenge of both groups with worm antigen. Despite the release of microgram quantities of RMCP-II into the gut lumen and vascular perfusate, however, there were no significant changes seen in the mucosal histology. These results suggest that RMCP-II alone is not responsible fore the loss of gut epithelium seen during anaphylaxis in the rat.
利用经颅肠系膜动脉对一段空肠进行离体灌注,研究了巴西日圆线虫致敏(免疫)大鼠空肠黏膜肥大细胞中大鼠肥大细胞蛋白酶-II(RMCP-II)的释放动力学。本研究的目的是评估该蛋白酶在过敏反应中的作用,特别是确定其是否与过敏反应体内模型中黏膜出现的组织学变化(包括广泛的上皮脱落)有关。用Krebs-Ringer缓冲液灌注空肠血管系统显示,在所有研究的大鼠中,空肠肥大细胞均有RMCP-II的基础分泌。与未接触过日圆线虫感染的对照、未致敏动物(<2 ng/ml)相比,先前接触过日圆线虫感染的免疫大鼠中RMCP-II的基线浓度显著更高(p<0.05)(>7 ng/ml)。用100或400条虫当量的全虫抗原攻击免疫大鼠,导致血管灌流液中RMCP-II的浓度立即(40秒内)显著升高(p<0.02)(至>3微克/ml),未致敏大鼠或用无关抗原攻击的免疫大鼠中未观察到这种情况。两组用虫抗原攻击后,与未致敏大鼠相比,免疫大鼠空肠腔中也回收了更多的RMCP-II。然而,尽管有微克量的RMCP-II释放到肠腔和血管灌流液中,但黏膜组织学未观察到显著变化。这些结果表明,单独的RMCP-II并不导致大鼠过敏反应期间所见的肠上皮丢失。