Cellular and molecular mechanisms for suppression of allergic response by dietary indigestible oligosaccharides

我们的目标是阐明α-半乳低聚糖(α-GOS)抑制过敏反应的细胞和分子机制。膳食α-GOS不能减少刀豆蛋白A诱导的小鼠肝炎和内毒素休克。体外培养的小鼠脾细胞可在脂多糖、抗原及NKT细胞的内源性和外源性配体刺激下产生干扰素-γ。由于抗CD1d抗体可抑制干扰素-γ的产生，CD1d限制性激活的NKT细胞可能与干扰素-γ的产生有关。但补充γ-GOS并不影响干扰素-γ的产生。这些结果提示α-GOS不影响NKT细胞的激活。饮食α-GOS可减少抗原攻击后小鼠腹膜细胞的渗出。饲料中添加α-GOS后，体外培养的小鼠腹膜渗出细胞和外周血白细胞对灌洗液的趋化性降低。然而，补充α-GOS并不影响趋化作用。因此，提示膳食α-GOS可降低某些趋化因子的表达。饮食中不可消化的低聚糖降低了半抗原诱导的小鼠接触超敏反应。由于抑制作用与盲肠双歧杆菌的数量有关，益生元可能会减少接触过敏等IV型过敏反应。

We aimed to clarify cellular and molecular mechanisms for suppression of allergic response by α-galactooligosaccharides (α-GOS).1. Dietary α-GOS did not reduce Con A-induced hepatitis and endotoxin shock in mice. IFN-γ production by mouse splenocytes ex vivo was stimulated by LPS, antigen, and endogenouse and exogenous ligands for NKT cells. Because the IFN-γ production was inhibited by anti-CD1d antibody, CD1d-restricted activation of NKT cells is probably responsible for the IFN-γ production. However, supplementation of γ-GOS did not affect the IFN-γ production. These findings suggest that α-GOS does not influence the activation of NKT cells.2. Dietary α-GOS reduced the infiltration of peritoneal cells after intraperitoneal challenge of antigen in primed mice. Chemotaxis of peritoneal exudate cells and peripheral leukocytes to peritoneal lavage fluid in vitro was also reduced by dietary α-GOS. However, supplementation of α-GOS did not affect the chemotaxis. It is therefore suggested that dietary α-GOS reduces the expression of some chemokines.3. Dietary non-digestible oligosaccharides reduced hapten-induced contact hypersensitivity in mice. Because the suppressive effect was correlated with the number of cecal bifidobacteria, prebiotics may reduce type IV allergic reactions such as contact hypersensitivity.