College of Animal Medicine, Northeast Agricultural University, Harbin 150030, China.
Food College, Northeast Agricultural University, Harbin 150030, China.
Food Funct. 2024 Nov 11;15(22):11252-11265. doi: 10.1039/d4fo03851g.
Human milk oligosaccharides (HMOs) and the milk fat globule membrane (MFGM) represent novel treatments for cow's milk allergy (CMA). They exhibit the beneficial attribute of diminishing nutrient damage when compared to conventional enzymatic digestion of milk proteins. However, the effects and mechanisms underlying the synergistic interaction between HMOs and the MFGM in allergy treatment remain unclear. Consequently, this study was undertaken to assess the protective properties of HMOs and the MFGM against CMA and to elucidate their potential mechanisms in a mouse model of β-lactoglobulin (BLG)-induced allergy. The findings demonstrated that HMOs and the MFGM could significantly reduce the allergy score and splenic index, and they diminished the levels of inflammatory mediators (total immunoglobulin E (IgE), specific IgE, histamine, and mMCP-1), while concurrently bolstering tight junctions (, , and ), and reducing intestinal permeability. Notably, HMOs and the MFGM exhibited optimal synergy. In addition, HMOs and the MFGM synergistically mitigated the immune response to Th2 overactivity in allergy by the promotion of Th1 and Treg cell responses, thereby suppressing the levels of inflammatory cytokines IL-4 and IL-5. Analysis of the gut microbiota and its metabolic activities revealed that HMOs and the MFGM increased the abundance of and , leading to higher production of butyrate. Furthermore, these beneficial bacteria and the resultant butyrate also contributed to the suppression of allergy-associated bacterial populations such as and . In summary, HMOs and the MFGM acted in synergy to modulate inflammatory responses and ameliorate barrier damage, contributing to the mitigation of CMA, a process potentially linked to gut microbiota dynamics and the resultant butyrate metabolism. This effect may be related to the gut microbiota and its metabolic production of butyrate.
人乳寡糖 (HMOs) 和乳脂肪球膜 (MFGM) 代表了牛奶过敏 (CMA) 的新型治疗方法。与传统的牛奶蛋白酶解相比，它们具有减少营养物质损伤的有益特性。然而，HMOs 和 MFGM 协同作用在过敏治疗中的效果和机制仍不清楚。因此，本研究旨在评估 HMOs 和 MFGM 对 CMA 的保护作用，并阐明它们在β-乳球蛋白 (BLG) 诱导的过敏小鼠模型中的潜在机制。研究结果表明，HMOs 和 MFGM 可显著降低过敏评分和脾脏指数，并降低炎症介质（总免疫球蛋白 E (IgE)、特异性 IgE、组胺和 mMCP-1）水平，同时增强紧密连接（，和），降低肠道通透性。值得注意的是，HMOs 和 MFGM 表现出最佳的协同作用。此外，HMOs 和 MFGM 通过促进 Th1 和 Treg 细胞反应来协同减轻过敏中 Th2 过度活跃的免疫反应，从而抑制炎症细胞因子 IL-4 和 IL-5 的水平。对肠道微生物群及其代谢活性的分析表明，HMOs 和 MFGM 增加了和的丰度，导致丁酸产量增加。此外，这些有益细菌和产生的丁酸也有助于抑制与过敏相关的细菌种群，如和。总之，HMOs 和 MFGM 协同作用调节炎症反应和改善屏障损伤，有助于减轻 CMA，这一过程可能与肠道微生物群动态及其产生的丁酸代谢有关。这种作用可能与肠道微生物群及其代谢产生的丁酸有关。
