Ju H R, Matsuura I, Yamada K, Sugano M, Imaizumi K
Department of Food Science and Technology, School of Agriculture (46-09), Kyushu University, Fukuoka, Japan.
Biosci Biotechnol Biochem. 1995 May;59(5):771-5. doi: 10.1271/bbb.59.771.
The plasma level of mucosal mast-cell protease was examined to find whether such measurements could be an indicator of allergic response to beta-lactoglobulin (beta-LG) challenged orally by rats. Brown Norway rats, which had been raised on a bovine milk-free diet, were systemically sensitized on day 0 with a low dose of beta-LG, and then by an oral administration of beta-LG for 3 h on day 14. The oral challenge with beta-LG in saline, when compared to saline alone, resulted in a systemic elevation of rat mast-cell protease II (RMCPII), one of the specific markers for gut mucosal mast-cell secretion. The challenge with beta-LG in a fat emulsion further increased the level of plasma RMCPII. This manipulation, however, was not successful for detecting any significant difference in mucosal leucotriene C4, another allergic mediator. An oral challenge with polymerized beta-LG did not induce any elevation of the protease, but resulted in a lower plasma level of beta-LG-specific IgG. This animal model is thus relevant to investigate the events regulating the mucosal hypersensitivity and humoral immunity to food proteins.
检测了黏膜肥大细胞蛋白酶的血浆水平，以确定此类测量是否可作为大鼠经口给予β-乳球蛋白（β-LG）后过敏反应的指标。将在无牛乳饮食中饲养的棕色挪威大鼠于第0天用低剂量的β-LG进行全身致敏，然后在第14天经口给予β-LG 3小时。与单独给予生理盐水相比，用生理盐水配制的β-LG经口激发可导致大鼠肥大细胞蛋白酶II（RMCPII）全身水平升高，RMCPII是肠道黏膜肥大细胞分泌的特异性标志物之一。用脂肪乳剂配制的β-LG激发可进一步提高血浆RMCPII水平。然而，这种操作未能成功检测到另一种过敏介质黏膜白三烯C4的任何显著差异。用聚合β-LG经口激发未引起蛋白酶水平升高，但导致β-LG特异性IgG的血浆水平降低。因此，该动物模型有助于研究调节对食物蛋白的黏膜超敏反应和体液免疫的相关事件。
