PDF(Pubmed)
Abstract：
It has become clear that the intestinal microbiota plays a role in food allergies. The objective of this study was to assess the food allergy-preventive effects of combined intake of a short fructan (1-kestose [Kes]) and a long fructan (inulin ([Inu]) in an ovalbumin (OVA)-induced food allergy mouse model.
Oral administration of fructans lowered the allergenic symptom score and alleviated the decreases in rectal temperature and total IgA levels and increases in OVA-specific IgE and IgA levels induced by high-dose OVA challenge, and in particular, combined intake of Kes and Inu significantly suppressed the changes in all these parameters. The expression of the pro-inflammatory cytokine IL-4, which was increased in the allergy model group, was significantly suppressed by fructan administration, and the expression of the anti-inflammatory cytokine IL-10 was significantly increased upon Kes administration. 16 S rRNA amplicon sequencing of the gut microbiota and beta diversity analysis revealed that fructan administration may induce gut microbiota resistance to food allergy sensitization, rather than returning the gut microbiota to a non-sensitized state. The relative abundances of the genera Parabacteroides B 862,066 and Alloprevotella, which were significantly reduced by food allergy sensitization, were restored by fructan administration. In Parabacteroides, the relative abundances of Parabacteroides distasonis, Parabacteroides goldsteinii, and their fructan-degrading glycoside hydrolase family 32 gene copy numbers were increased upon Kes or Inu administration. The concentrations of short-chain fatty acids (acetate and propionate) and lactate were increased by fructan administration, especially significantly in the Kes + Inu, Kes, and Inu-fed (Inu, Kes + Inu) groups.
Combined intake of Kes and Inu suppressed allergy scores more effectively than single intake, suggesting that Kes and Inu have different allergy-preventive mechanisms. This indicates that the combined intake of these short and long fructans may have an allergy-preventive benefit.
Oral administration of fructans lowered the allergenic symptom score and alleviated the decreases in rectal temperature and total IgA levels and increases in OVA-specific IgE and IgA levels induced by high-dose OVA challenge, and in particular, combined intake of Kes and Inu significantly suppressed the changes in all these parameters. The expression of the pro-inflammatory cytokine IL-4, which was increased in the allergy model group, was significantly suppressed by fructan administration, and the expression of the anti-inflammatory cytokine IL-10 was significantly increased upon Kes administration. 16 S rRNA amplicon sequencing of the gut microbiota and beta diversity analysis revealed that fructan administration may induce gut microbiota resistance to food allergy sensitization, rather than returning the gut microbiota to a non-sensitized state. The relative abundances of the genera Parabacteroides B 862,066 and Alloprevotella, which were significantly reduced by food allergy sensitization, were restored by fructan administration. In Parabacteroides, the relative abundances of Parabacteroides distasonis, Parabacteroides goldsteinii, and their fructan-degrading glycoside hydrolase family 32 gene copy numbers were increased upon Kes or Inu administration. The concentrations of short-chain fatty acids (acetate and propionate) and lactate were increased by fructan administration, especially significantly in the Kes + Inu, Kes, and Inu-fed (Inu, Kes + Inu) groups.
Combined intake of Kes and Inu suppressed allergy scores more effectively than single intake, suggesting that Kes and Inu have different allergy-preventive mechanisms. This indicates that the combined intake of these short and long fructans may have an allergy-preventive benefit.
摘要：
背景：很明显，肠道微生物群在食物过敏中起作用。这项研究的目的是评估在卵清蛋白（OVA）中联合摄入短果聚糖（1-kestose[Kes]）和长果聚糖（菊粉（[Inu]）的食物过敏预防作用。食物过敏小鼠模型。
结果：口服果聚糖降低了变应原症状评分，减轻了高剂量OVA激发引起的直肠温度和总IgA水平的下降以及OVA特异性IgE和IgA水平的升高，特别是,Kes和Inu的联合摄入显著抑制了所有这些参数的变化。致炎细胞因子IL-4的表达在变态反应模型组中增加,被果聚糖给药显著抑制，抗炎性细胞因子IL-10的表达在Kes给药后显著增加。16SrRNA扩增子对肠道菌群的测序和β多样性分析显示，果聚糖给药可诱导肠道菌群抵抗食物过敏致敏，而不是将肠道微生物群恢复到非致敏状态。副杆菌属B862,066和Alloprevotella的相对丰度，食物过敏致敏显著降低，通过果聚糖管理恢复。在副杆菌属中，Distasonis副杆菌属的相对丰度，金氏副杆菌,Kes或Inu施用后，其果聚糖降解糖苷水解酶家族32基因拷贝数增加。短链脂肪酸（乙酸盐和丙酸盐）和乳酸的浓度通过果聚糖给药增加，尤其是在Kes+Inu中，Kes,和Inu-fed(Inu，Kes+Inu)组。
结论：Kes和Inu的联合摄入比单次摄入更有效地抑制了过敏评分，表明Kes和Inu有不同的过敏预防机制。这表明这些短果聚糖和长果聚糖的联合摄入可能具有预防过敏的益处。
结果：口服果聚糖降低了变应原症状评分，减轻了高剂量OVA激发引起的直肠温度和总IgA水平的下降以及OVA特异性IgE和IgA水平的升高，特别是,Kes和Inu的联合摄入显著抑制了所有这些参数的变化。致炎细胞因子IL-4的表达在变态反应模型组中增加,被果聚糖给药显著抑制，抗炎性细胞因子IL-10的表达在Kes给药后显著增加。16SrRNA扩增子对肠道菌群的测序和β多样性分析显示，果聚糖给药可诱导肠道菌群抵抗食物过敏致敏，而不是将肠道微生物群恢复到非致敏状态。副杆菌属B862,066和Alloprevotella的相对丰度，食物过敏致敏显著降低，通过果聚糖管理恢复。在副杆菌属中，Distasonis副杆菌属的相对丰度，金氏副杆菌,Kes或Inu施用后，其果聚糖降解糖苷水解酶家族32基因拷贝数增加。短链脂肪酸（乙酸盐和丙酸盐）和乳酸的浓度通过果聚糖给药增加，尤其是在Kes+Inu中，Kes,和Inu-fed(Inu，Kes+Inu)组。
结论：Kes和Inu的联合摄入比单次摄入更有效地抑制了过敏评分，表明Kes和Inu有不同的过敏预防机制。这表明这些短果聚糖和长果聚糖的联合摄入可能具有预防过敏的益处。
