Bifidobacterium bifidum FB3-12 attenuates ovalbumin-induced allergic diseases by enhancing intestinal barrier function and regulating gut microbiota

双歧杆菌FB3-12通过增强肠道屏障功能和调节肠道菌群来减轻卵清蛋白诱发的过敏性疾病。

阅读:1

Abstract

The escalating environmental changes have exacerbated the physiological suffering and economic burden caused by allergic diseases worldwide. Bifidobacterium bifidum (B. bifidum), due to its positive regulatory effects on the gut microenvironment, is considered a promising strategy for the prevention and treatment of allergies. Our study utilized the ovalbumin (OVA)-induced allergy mouse model to explore the anti-allergic potential of the self-screened strain B. bifidum FB3-12 (FB3-12) via intestinal intervention. The results demonstrated that a three-week FB3-12 treatment effectively suppressed the levels of immune markers, including OVA-specific immunoglobulin E (OVA-sIgE), mast cell protease-1 (Mcpt-1), and histamine (HIS) in the serum of allergic mice, and restored the Th2/Th1 immune response imbalance in the spleen. Furthermore, compared to the OVA group, FB3-12 intervention ameliorated intestinal damage and inflammation, significantly increasing the relative expression of Mucin-2 and tight junction proteins. Analysis of the gut microbiota profile revealed a distinct shift in the enterotype of OVA-challenged mice, characterized by a decreased Firmicutes/Bacteroidetes (F/B) ratio and a marked increase in the relative abundance of Akkermansia. FB3-12 intervention significantly enriched beneficial genera such as Lactobacillus and Colidextribacter, and upregulated the levels of short-chain fatty acids (SCFAs) and associated G protein-coupled receptors (GPRs) in the intestine. These findings underscore the therapeutic potential and application value of FB3-12 in alleviating allergic diseases through modulation of the gut microbiome.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。