Dietary oligofructose and inulin protect mice from enteric and systemic pathogens and tumor inducers
Dietary oligofructose and inulin protect mice from enteric and systemic pathogens and tumor inducers
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DOI：
10.1093/jn/132.3.472
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发表时间：
2002-03-01
影响因子：
4.2
通讯作者：
Buddington, RK
中科院分区：
文献类型：
--
作者：
Buddington, KK;Donahoo, JB;Buddington, RK
益生素可以改变胃肠道细菌的数量和代谢特征，调节肠道和全身免疫功能，并使实验室啮齿动物对促进结直肠癌的致癌物具有抵抗力。关于如何保护自己免受其他挑战的影响，人们知之甚少。因此，将B6C3F1品系的小鼠饲喂含100g/kg纤维素的对照饲料或两种试验性饲料中的一种，其中一种是完全由非可消化低聚糖(NDO)、低聚果糖和菊粉取代。在每种饮食中，25只小鼠接受结直肠癌促进剂(1，2-二甲基肼)、B16F10肿瘤细胞、肠道病原体白色念珠菌的攻击，或者系统感染单核细胞增多性李斯特菌或鼠伤寒沙门氏菌。灌胃菊粉(53%)和低聚果糖(54%)的小鼠在染毒后远端结肠出现异常隐窝病灶的发生率低于对照组(76%；P<；0.05)，但果糖并不能降低注射B16F10肿瘤细胞后小鼠的肺癌发生率。喂食果糖的小鼠小肠中白色念珠菌的密度降低了50%(P<；0.05)。单核细胞增多性李斯特氏菌的全身感染在对照组小鼠中造成了近30%的死亡，但饲喂菊粉的小鼠无一死亡，而饲喂低聚果糖的小鼠的存活介于两者之间。全身感染鼠伤寒沙门氏菌的死亡率较高(对照组小鼠死亡率为80%)，但喂食菊粉的小鼠死亡率较低(60%；P<；0.05)，而喂食低聚果糖的小鼠死亡率又居中。膳食NDO增加抵抗力的机制尚未阐明，但这一发现与免疫功能增强是一致的，以应对驻留在胃肠道的细菌组成和代谢特征的变化。
Prebiotics induce changes in the population and metabolic characteristics of the gastrointestinal bacteria, modulate enteric and systemic immune functions, and provide laboratory rodents with resistance to carcinogens that promote colorectal cancer. There is less known about protection from other challenges. Therefore, mice of the B6C3F1 strain were fed for 6 wk a control diet with 100 g/kg cellulose or one of two experimental diets with the cellulose replaced entirely by the nondigestible oligosaccharides (NDO) oligofructose and inulin. From each diet, 25 mice were challenged by a promoter of colorectal cancer (1,2-dimethylhydrazine), B16F10 tumor cells, the enteric pathogen Candida albicans (enterically), or were infected systemically with Listeria monocytogenes or Salmonella typhimurium. The incidences of aberrant crypt foci in the distal colon after exposure to dimethylhdrazine for mice fed inulin (53%) and oligofructose (54%) were lower than in control mice (76%; P < 0.05), but the fructans did not reduce the incidence of lung tumors after injection of the B16F10 tumor cells. Mice fed the diets with fructans had 50% lower densities of C. albicans in the small intestine (P < 0.05). A systemic infection with L. monocytogenes caused nearly 30% mortality among control mice, but none of the mice fed inulin died, with survival intermediate for mice fed oligofructose. Mortality was higher for the systemic infection of S. typhimurium (>80% for control mice), but fewer of the mice fed inulin died (60%; P < 0.05), with mice fed oligofructose again intermediate. The mechanistic basis for the increased resistance provided by dietary NDO was not elucidated, but the findings are consistent with enhanced immune functions in response to changes in the composition and metabolic characteristics of the bacteria resident in the gastrointestinal tract.