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动物双歧杆菌乳亚种BX-BC08调节肠道微生物群并分泌α-酮戊二酸以减轻MC903诱导的特应性皮炎。

Bifidobacterium animalis subsp. Lactis BX-BC08 modulates gut microbiota and secretes alpha-Ketoglutaric acid to alleviate MC903-induced atopic dermatitis.

作者信息

Zhao Jiamin, Kui Ling, Huang Jinqun, Deng Jie, Liu Lingjun, Zhu Chenwei, Shi Yanqiang, Li Chengyi, Xiao Yue, Yu Jinshi, Li Qing, Yang Bin, Leng Bingfeng, Chan Hung

机构信息

Dermatology Hospital, Southern Medical University, Guangzhou, China.

Hong Kong Rising Biotechnology Co. Limited, Hong Kong, China.

出版信息

J Transl Med. 2025 Jul 10;23(1):768. doi: 10.1186/s12967-025-06769-9.

Abstract

OBJECTIVE

Bifidobacterium is known to be depleted in patients with atopic dermatitis (AD). This study aims to investigate the potential prophylactic effects of Bifidobacterium animalis subsp. lactis BX-BC08 (B. lactis BX-BC08) in a murine model of AD.

DESIGN

The immunosuppressive and anti-inflammatory effects of BX-BC08 were evaluated in a MC903-induced AD mouse model. Gut microbiota composition was analyzed by metagenomic sequencing, while high-performance liquid chromatography-mass spectrometry (HPLC-MS) was employed to identify anti-inflammatory molecules produced by B. lactis BX-BC08.

RESULTS

BX-BC08 significantly attenuated pro-inflammatory responses, scaling and swelling in the MC903-induced AD like murine model compared to controls. Fecal microbial profiling revealed an enrichment of probiotics and a reduction of pro-inflammatory bacteria in BX-BC08 treated mice. Metabolic analysis of BX-BC08 bacteria culture supernatant and treated mice identified a significant enrichment of alpha-Ketoglutaric acid (AKG). Functional validation in the murine AD model demonstrated that AKG strongly suppressed T helper 2 (Th2)-driven pro-inflammatory responses.

CONCLUSION

BX-BC08 mitigates AD-like inflammation by producing the anti-inflammatory metabolite AKG. BX-BC08 could serve as a novel prophylactic agent for AD prevention.

摘要

目的

已知双歧杆菌在特应性皮炎(AD)患者中数量减少。本研究旨在调查动物双歧杆菌乳酸亚种BX-BC08(B. lactis BX-BC08)在AD小鼠模型中的潜在预防作用。

设计

在MC903诱导的AD小鼠模型中评估BX-BC08的免疫抑制和抗炎作用。通过宏基因组测序分析肠道微生物群组成,同时采用高效液相色谱-质谱联用(HPLC-MS)鉴定B. lactis BX-BC08产生的抗炎分子。

结果

与对照组相比,BX-BC08在MC903诱导的类AD小鼠模型中显著减轻了促炎反应、脱屑和肿胀。粪便微生物谱分析显示,经BX-BC08处理的小鼠中益生菌富集,促炎细菌减少。对BX-BC08细菌培养上清液和处理过的小鼠进行代谢分析,发现α-酮戊二酸(AKG)显著富集。在小鼠AD模型中的功能验证表明,AKG强烈抑制辅助性T细胞2(Th2)驱动的促炎反应。

结论

BX-BC08通过产生抗炎代谢物AKG减轻类AD炎症。BX-BC08可作为预防AD的新型预防剂。

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