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短双歧杆菌 M-16V 通过 IL-33/ST2 信号通路改变肠道微生物群缓解卵清蛋白诱导的食物过敏。

Bifidobacterium breve M-16V alters the gut microbiota to alleviate OVA-induced food allergy through IL-33/ST2 signal pathway.

机构信息

Department of Pediatric, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Institute of tropical medicine, Hainan Medical University, HaiKou, China.

出版信息

J Cell Physiol. 2020 Dec;235(12):9464-9473. doi: 10.1002/jcp.29751. Epub 2020 May 11.

Abstract

There has been a marked increase in life-threatening food allergy (FA). One hypothesis is that changes in bacterial communities may be key to FA. To better understand how gut microbiota regulates FA in humans, we established a mouse model with FA induced by ovalbumin. We found that the mice with FA had abnormal bacterial composition, accompanied by increased immunoglobulin G, immunoglobulin E, and interleukin-4/interferon-γ, and there existed a certain coherence between them. Interestingly, Bifidobacterium breve M-16V may alter the gut microbiota to alleviate the allergy symptoms by IL-33/ST2 signaling. Our results indicate that gut microbiota is essential for regulating FA to dietary antigens and demonstrate that intervention in bacterial community regulation may be therapeutically related to FA.

摘要

食物过敏(FA)的致死率显著增加。有一种假说认为,细菌群落的变化可能是 FA 的关键。为了更好地理解肠道微生物群如何调节人类的 FA,我们建立了一种由卵清蛋白诱导的 FA 小鼠模型。我们发现,FA 小鼠的细菌组成异常,同时免疫球蛋白 G、免疫球蛋白 E 和白细胞介素-4/干扰素-γ增加,且它们之间存在一定的一致性。有趣的是,短双歧杆菌 M-16V 可能通过 IL-33/ST2 信号改变肠道微生物群来缓解过敏症状。我们的结果表明,肠道微生物群对于调节对膳食抗原的 FA 至关重要,并证明干预细菌群落调节可能与 FA 具有治疗相关性。

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