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

我们旨在阐明α-半乳糖低聚糖（α-GOS）抑制过敏反应的细胞和分子机制。饲粮α-GOS对Con - a诱导的小鼠肝炎和内毒素休克无明显影响。LPS、抗原、内源性和外源性配体刺激小鼠脾细胞体外产生IFN-γ。由于抗cd1d抗体抑制IFN-γ的产生，cd1d限制的NKT细胞激活可能是IFN-γ产生的原因。然而，补充γ-GOS不影响IFN-γ的产生。这些结果表明α-GOS不影响NKT细胞的活化。饲粮α-GOS可减少抗原注入小鼠腹膜后腹膜细胞的浸润。α-GOS还能降低体外培养的腹膜渗出细胞和外周血白细胞对腹腔灌洗液的趋化性。然而，补充α-GOS不影响趋化性。因此，饲粮α-GOS可降低部分趋化因子的表达。饮食中不可消化低聚糖可减少小鼠半抗原诱导的接触性超敏反应。由于这种抑制作用与盲肠双歧杆菌的数量有关，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.