Oral administration of a galactooligosaccharide preparation inhibits development of atopic dermatitis-like skin lesions in NC/Nga mice

Oral administration of a galactooligosaccharide preparation inhibits development of atopic dermatitis-like skin lesions in NC/Nga mice
复制标题

DOI:
10.3892/ijmm_00000349
复制
发表时间:
2010-03-01
影响因子:
5.4
通讯作者:
Hochi, Satomi
Hochi, Satomi
中科院分区:
医学3区
文献类型:
--
作者:
Tanabe, Soichi;Hochi, Satomi

文献摘要

被引文献

相似文献

半乳糖低聚糖(GOS)存在于母乳中,经常添加到食物中以促进健康,研究人员在异位性皮炎(AD)的类人小鼠模型中评估了GOS的抗过敏作用。NC/Nga小鼠喂食5.5% GOS 8周,我们检测这种处理是否抑制了这些小鼠ad样皮肤病变的发展。与对照组相比,喂食GOS的小鼠皮炎症状明显减轻,抓挠频率减少,血清总免疫球蛋白E水平降低。8周实验结束时,取脾,用12-肉豆蔻酸13-乙酸佛波和离子霉素刺激脾细胞,分析细胞因子和趋化因子的产生。在gos喂养小鼠的脾细胞中观察到Th1细胞因子如干扰素γ水平升高。然而,Th2细胞因子如白细胞介素(IL)-13的水平没有变化。此外,GOS抑制炎症细胞因子如IL-1 β、IL-6、IL-17和肿瘤坏死因子的产生,但增强免疫调节性IL-10的产生。结果表明,GOS通过至少部分诱导IL-10的产生和抑制IL-17等参与皮肤炎症的细胞因子的产生,有效地阻断小鼠ad样皮肤病变。
Anti-allergic effects of galactooligosaccharide (GOS), which is found in breast milk and frequently added to food for promoting health, were evaluated in a human-like mouse model of atopic dermatitis (AD). NC/Nga mice were fed 5.5% GOS for 8 weeks, and we examined whether this treatment suppressed the development of AD-like skin lesions in these mice. Mice fed GOS exhibited significantly less symptoms of dermatitis, reduced scratching frequency, and lower levels of serum total immunoglobulin E compared to control. At the end of the 8-week-experimental period, spleens were removed, and the splenocytes were stimulated with phorbol 12-myristate 13-acetate and ionomycin, following which production of cytokines and a chemokine was analyzed. Elevated levels of Th1 cytokines such as interferon-gamma were observed in splenocytes from GOS-fed mice. However, the levels of Th2 cytokines such as interleukin (IL)-13 were unchanged. Furthermore, GOS inhibited the production of inflammatory cytokines such as IL-1 beta, IL-6, IL-17, and tumor necrosis factor-a but enhanced production of immunomodulatory IL-10. The results indicate that GOS effectively blocked AD-like skin lesions in the mice by at least partly inducing production of IL-10 and suppressing the production of cytokines such as IL-17, which are involved in skin inflammation.