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

本研究旨在阐明α-低聚半乳糖（α-GOS）抑制过敏反应的细胞和分子机制.α-GOS不能减轻Con A诱导的小鼠肝炎和内毒素休克。用LPS、抗原、NKT细胞的内源性和外源性配体刺激小鼠脾细胞离体产生IFN-γ。由于IFN-γ的产生受到抗CD 1d抗体的抑制，因此CD 1d限制性激活NKT细胞可能是IFN-γ产生的原因。而添加γ-GOS对IFN-γ的产生无影响。提示α-GOS不影响NKT细胞的活化.α-GOS可减少抗原腹腔内攻击后腹腔细胞的浸润。α-GOS还可降低腹腔渗出液细胞和外周血白细胞对腹腔灌洗液的趋化性。而α-GOS的添加对趋化性无影响。因此，膳食α-GOS降低了某些趋化因子的表达.饮食中的非消化性低聚糖降低了小鼠半抗原诱导的接触性超敏反应。由于抑制效果与盲肠细菌数量相关，益生元可能会减少IV型过敏反应，如接触性超敏反应。

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.