Gee J M, Wal J M, Miller K, Atkinson H, Grigoriadou F, Wijnands M V, Penninks A H, Wortley G, Johnson I T
Institute of Food Research, Norwich Laboratory, Norfolk, UK.
Toxicology. 1997 Feb 28;117(2-3):219-28. doi: 10.1016/s0300-483x(96)03574-3.
The ability of saponins and glycoalkaloids to permeabilise the mammalian intestinal barrier has been previously demonstrated in vitro, leading to the hypothesis that membranolytic saponins may facilitate transfer to the tissues of otherwise excluded macromolecules. An enhanced uptake of, for instance, potentially allergenic species from the lumen is one of the factors that may affect the induction of food allergy, and its presentation in already sensitised individuals. In the experiments described here, an increase in the transmucosal uptake of the milk allergen beta-lactoglobulin (beta LG) was assessed in non-sensitised and sensitised Brown Norway rats in the presence of Gypsophila saponin. Isolated jejunal loops were exposed in vivo to either beta LG followed by saponin, saponin followed by beta LG or the two compounds simultaneously. Portal vein blood samples were collected and assayed for beta LG and rat mucosal mast cell protease (RCMP II) activity. Mucosal tissue was also examined histologically and assayed for histamine content. Sham-operated animals, exposed to physiological buffer alone, were included as controls and beta LG measurements corrected for this component which was negligible. No transfer of beta LG occurred in the absence of saponin in non-sensitised rats, whereas a significant enhancement was observed in the presence of saponin. beta LG was detected in the portal circulation of sensitised rats exposed to beta LG alone; however addition of saponin to the intestinal lumen further enhanced this uptake, possibly by an independent mechanism. Histological examination of the mucosal epithelium exposed to saponin revealed damage, especially at the villus tips. Mucosal histamine and serum RCMP II concentrations were consistent with the differences observed between sensitised and non-sensitised animals. It is concluded that exposure to food constituents capable of permeabilising the mucosal epithelium may increase the risk of sensitisation to dietary antigens.
皂苷和糖苷生物碱使哺乳动物肠道屏障通透性增加的能力先前已在体外得到证实，由此提出一种假说，即具有膜溶解作用的皂苷可能有助于原本无法进入的大分子转移至组织。例如，管腔中潜在过敏原的摄取增加是可能影响食物过敏诱导及其在已致敏个体中表现的因素之一。在此处描述的实验中，评估了在满天星皂苷存在的情况下，未致敏和已致敏的棕色挪威大鼠对牛奶过敏原β-乳球蛋白（β-LG）经黏膜摄取的增加情况。将分离的空肠袢在体内暴露于β-LG后再给予皂苷、先给予皂苷后给予β-LG或同时给予这两种化合物。采集门静脉血样本并检测其中β-LG和大鼠黏膜肥大细胞蛋白酶（RCMP II）活性。还对黏膜组织进行了组织学检查并检测组胺含量。仅暴露于生理缓冲液的假手术动物作为对照，对β-LG测量值进行了校正，因为该成分可忽略不计。在未致敏大鼠中，不存在皂苷时β-LG不会发生转移，而存在皂苷时则观察到显著增强。单独暴露于β-LG的已致敏大鼠的门静脉循环中检测到了β-LG；然而，向肠腔中添加皂苷进一步增强了这种摄取，可能是通过一种独立机制。对暴露于皂苷的黏膜上皮进行组织学检查发现有损伤，尤其是在绒毛尖端。黏膜组胺和血清RCMP II浓度与已致敏和未致敏动物之间观察到的差异一致。得出的结论是，暴露于能够使黏膜上皮通透性增加的食物成分可能会增加对饮食抗原致敏的风险。
