Screening of factors triggering food allergy and research on development of hypoallergic food products.

本实验测定了不同环境化学物β-六六六（beta-BHC）、对，对'-二氯二苯二氯乙烯（DDE）、对硝基苯基2，4，6-三氯苯基醚（CNP）、D-α-氨基苄青霉素（D-alpha-aminobenzylpenicillin）、邻乙酰柠檬酸三丁酯（o-acetylcitricacidtubyl ester，ATBC）对免疫应答的影响。所有的化学物质都会影响淋巴结细胞对抗原的反应，从而影响细胞因子的分泌。化学品也影响口服抗原引起的血清抗体反应。用卵清蛋白（OVA）诱导T细胞受体转基因小鼠脾白细胞介素（IL）-4分泌细胞和血清IgE抗体应答。接下来，该系统用于检查化学物质对与过敏反应相关的免疫反应的影响。结果表明，ATBC可抑制IL-4的产生。此外，测试了参与脂质代谢的物质对来自这些T细胞受体转基因小鼠的T细胞的细胞因子分泌的影响。亚油酸和花生四烯酸抑制IL-4的分泌。此外，我们还研究了干酪乳杆菌（Lactobacillus casei）对抗原诱导的IgE分泌的影响。干酪乳杆菌通过诱导巨噬细胞分泌IL-12来抑制IgE的产生。结果表明，这种生物体在预防IgE介导的过敏中具有潜在的用途。

We tested the effects of various environmental chemicals, beta-benzene hexachloride (beta-BHC), p, p'-dichlorodiphenyldichloroethylene (DDE), p-nitrophenyl 2, 4, 6-trichiorophenyl ether (CNP), D-alpha-aminobenzylpenicillin (Amp), o-acetylcitricacidtributyl ester (ATBC) on the immune response. All of the chemicals affectedcytokine secretion by lymph node cells in response to antigen. The chemicals also affected the serum antibody response elicited by oral administration of antigen. Feeding ovalbumin (OVA) to OVA-specific T cell receptor transgenic mice inducedinterleukin (IL)-4-secreting cells in the spleen and a serum IgE antibody response. Next this system was used to examine the effect of chemicals on immune responses related to allergic reactions. It was found that ATBC inhibited IL-4-production in this system. Further, substances involved in lipid metabolism were tested for their effect on cytokine secretion of T cells from these T cell receptor transgenic mice. Linoleic acid and arachidonic acid inhibited IL-4 secretion. These experimental systems should be useful for screening of factors affecting immune responses in food stuff.In addition, the effect of Lactobacillus casei, a nonpathogenic bacterium used in dairy products on antigen-induced IgE secretion was tested L.casei inhibited IgE production through induction of IL-12 secretion by macrophages. The results suggest a potential use of this organism in preventing IgE-mediated allergy.