Details

Autor(en) / Beteiligte

• Li, Na
• Yu, Yi
• Chen, Xuehua
• Gao, Shenshen
• Zhang, Qingqing
• Xu, Chundi

Titel

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

Ist Teil von

• Journal of cellular physiology, 2020-12, Vol.235 (12), p.9464-9473

Ort / Verlag

United States: Wiley Subscription Services, Inc

Erscheinungsjahr

2020

Quelle

Wiley Blackwell Single Titles

Beschreibungen/Notizen

• 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. Food allergy (FA) has emerged as a life‐threatening disease worldwide with gastrointestinal damage. The imbalance of intestinal flora and immune response are related to food sensitivities. It is found that the interleukin‐33/suppression of tumorigenicity 2 pathway may involve the occurrence and development of allergic diseases. This study aimed to examine the relationships among gut microbiota, immune function, and FA, and evaluate the potential of an oral exposure to Bifidobacterium breve M‐16V (Bb M‐16V) to relieve allergy symptoms in a mouse model of FA. The results seek to provide a new basis for the application of Bb M‐16V in FA and reveal the vital function of different intestinal microbiota composition after exposure to allergen in regulating T cell responses to intestinal allergic reactivity.