Bhatia S K, Rose N R, Schofield B, Lafond-Walker A, Kuppers R C
Department of Molecular Microbiology & Immunology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA.
Proc Soc Exp Biol Med. 1996 Dec;213(3):294-300. doi: 10.3181/00379727-213-44062.
Immunization of CBA/J mice with thryoglobulin (Tg) emulsified in complete Freund's adjuvant induces experimental thyroiditis (EAT), a well-characterized model of Hashimoto's disease. Recent studies have suggested that dietary factors play a role in the modulation of the immune response and that diet can have a profound effect on the induction of autoimmune diseases. In this study, we examined the influence of diet on autoimmune thyroiditis in mice. EAT was induced in mice fed ad libitum one of the three diets, a standard maintenance chow (Agway H1000), Purina 5020 Breeding Chow, and Purina 5010 Autoclavable (unautoclaved) Diet. Tg-immunized mice fed the Agway 1000 diet were found to be resistant to the development of autoimmune thyroid disease, with only 4 out of 25 mice developing mild thyroiditis. In contrast, 16 out of 25 mice fed the Purina 5010 diet developed moderate to severe thyroiditis. Mice fed the 5020 diet were partly susceptible: 7 out of 25 developed a mild to moderate thyroiditis. Histologic examination of thyroid glands of diseased mice fed the 5010 and 5020 diets showed marked lymphocytic infiltration with destruction of follicles, compared with mice fed the Agway diet, the latter showing only mild infiltration with preservation of thyroid follicles. Titers of antibody to Tg did not differ among the groups, and there was no significant difference in the IgG isotype subclass usage. The results demonstrate that diet can markedly affect the severity of autoimmune disease in the EAT model. In contrast, diet has little effect on the humoral autoimmune response in this system. These results implicate diet as a factor in the severity of cell-mediated autoimmune destruction and suggest that dietary modification could decrease pathology in some forms of autoimmune disease.
用完全弗氏佐剂乳化的甲状腺球蛋白(Tg)免疫CBA/J小鼠可诱发实验性甲状腺炎(EAT),这是一种特征明确的桥本氏病模型。最近的研究表明,饮食因素在免疫反应调节中起作用,并且饮食对自身免疫性疾病的诱发可能产生深远影响。在本研究中,我们检测了饮食对小鼠自身免疫性甲状腺炎的影响。随意喂食三种饮食(标准维持饲料(Agway H1000)、普瑞纳5020繁殖饲料和普瑞纳5010可高压灭菌(未高压灭菌)饲料)之一的小鼠诱发了EAT。发现喂食Agway 1000饲料的Tg免疫小鼠对自身免疫性甲状腺疾病的发展具有抗性,25只小鼠中只有4只发生轻度甲状腺炎。相比之下,喂食普瑞纳5010饲料的25只小鼠中有16只发生中度至重度甲状腺炎。喂食5020饲料的小鼠部分易感:25只中有7只发生轻度至中度甲状腺炎。与喂食Agway饲料的小鼠相比,喂食5010和5020饲料的患病小鼠甲状腺组织学检查显示有明显的淋巴细胞浸润和滤泡破坏,后者仅表现为轻度浸润且甲状腺滤泡保存。各组Tg抗体滴度无差异,IgG同种型亚类使用情况也无显著差异。结果表明,饮食可显著影响EAT模型中自身免疫性疾病的严重程度。相比之下,饮食对该系统中的体液自身免疫反应影响很小。这些结果表明饮食是细胞介导的自身免疫破坏严重程度的一个因素,并提示饮食调整可能减轻某些形式自身免疫性疾病的病理变化。