Hilton J, Dearman R J, Basketter D A, Kimber I
Zeneca Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire, UK.
Toxicol Lett. 1994 Jul;73(1):43-53. doi: 10.1016/0378-4274(94)90187-2.
It is known that a variety of materials, including both low molecular weight chemicals and proteins, is able to induce occupational respiratory allergy. We have shown previously that exposure of mice to chemical respiratory sensitizers results in both a marked increase in the serum concentration of IgE and the appearance of specific IgE antibody. In the present study we have examined the characteristics of immune responses induced in mice following intraperitoneal exposure to 3 protein respiratory allergens, ovalbumin (OVA), a lipase from Aspergillus oryzae (LP) and an amylase from Bacillus subtilis (AM) and to a fourth protein, bovine serum albumin (BSA), which is considered usually not to cause respiratory sensitization. Under conditions where all proteins provoked IgG antibody responses, only OVA, LP and AM elicited specific IgE antibody. As judged by passive cutaneous anaphylaxis (PCA) assay, BSA failed to induce an IgE response. In contrast to chemical respiratory sensitizers, the protein allergens examined here failed to cause a substantial increase in the serum concentration of IgE; OVA and AM induced no increase in serum IgE and LP only a comparatively modest increase relative to control values. In conclusion, these data demonstrate that while protein respiratory allergens are able to provoke specific IgE antibody, they fail to cause a marked increase in the concentration of this immunoglobulin in the sera of treated mice. It would appear, therefore, that the mouse IgE test, which seeks to evaluate chemical respiratory sensitization potential as a function of induced changes in the concentration of serum IgE, will be inappropriate for the identification of protein respiratory allergens. Nevertheless, identification of protein allergens may be possible by exploiting the observations reported here that such proteins induce in mice specific IgE antibody responses.
众所周知，包括低分子量化学物质和蛋白质在内的多种物质都能够诱发职业性呼吸道过敏。我们之前已经表明，将小鼠暴露于化学性呼吸道致敏剂会导致血清IgE浓度显著升高以及特异性IgE抗体的出现。在本研究中，我们检测了小鼠经腹腔注射三种蛋白质呼吸道变应原（卵清蛋白（OVA）、米曲霉脂肪酶（LP）和枯草芽孢杆菌淀粉酶（AM））以及第四种蛋白质牛血清白蛋白（BSA）（通常认为其不会引起呼吸道致敏）后诱导的免疫反应特征。在所有蛋白质都引发IgG抗体反应的条件下，只有OVA、LP和AM引发了特异性IgE抗体。通过被动皮肤过敏反应（PCA）试验判断，BSA未能诱导IgE反应。与化学性呼吸道致敏剂不同，此处检测的蛋白质变应原未能使血清IgE浓度大幅升高；OVA和AM未引起血清IgE升高，LP仅相对于对照值有相对适度的升高。总之，这些数据表明，虽然蛋白质呼吸道变应原能够引发特异性IgE抗体，但它们未能使处理过的小鼠血清中这种免疫球蛋白的浓度显著升高。因此，似乎旨在根据血清IgE浓度的诱导变化来评估化学性呼吸道致敏潜力的小鼠IgE试验不适用于鉴定蛋白质呼吸道变应原。然而，利用此处报道的这些蛋白质在小鼠中诱导特异性IgE抗体反应的观察结果，有可能鉴定出蛋白质变应原。
