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抗生素诱导的肠道微生物失调破坏肠道屏障,增加成年小鼠的食物过敏。

Antibiotic-Induced Gut Microbiota Dysbiosis Damages the Intestinal Barrier, Increasing Food Allergy in Adult Mice.

机构信息

Key Laboratory of Precision Nutrition and Food Quality, Key Laboratory of Functional Dairy, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.

出版信息

Nutrients. 2021 Sep 23;13(10):3315. doi: 10.3390/nu13103315.


DOI:10.3390/nu13103315
PMID:34684316
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8539551/
Abstract

(1) Background: The use of antibiotics affects the composition of gut microbiota. Studies have suggested that the colonization of gut microbiota in early life is related to later food allergies. Still, the relationship between altered intestinal microbiota in adulthood and food allergies is unclear. (2) Methods: We established three mouse models to analyze gut microbiota dysbiosis' impact on the intestinal barrier and determine whether this effect can increase the susceptibility to and severity of food allergy in later life. (3) Results: The antibiotic-induced gut microbiota dysbiosis significantly reduced Lachnospiraceae, Muribaculaceae, and Ruminococcaceae, and increased Enterococcaceae and Clostridiales. At the same time, the metabolic abundance was changed, including decreased short-chain fatty acids and tryptophan, as well as enhanced purine. This change is related to food allergies. After gut microbiota dysbiosis, we sensitized the mice. The content of specific IgE and IgG1 in mice serum was significantly increased, and the inflammatory response was enhanced. The dysbiosis of gut microbiota caused the sensitized mice to have more severe allergic symptoms, ruptured intestinal villi, and a decrease in tight junction proteins (TJs) when re-exposed to the allergen. (4) Conclusions: Antibiotic-induced gut microbiota dysbiosis increases the susceptibility and severity of food allergies. This event may be due to the increased intestinal permeability caused by decreased intestinal tight junction proteins and the increased inflammatory response.

摘要

(1)背景:抗生素的使用会影响肠道微生物群的组成。研究表明,早期肠道微生物群的定植与以后的食物过敏有关。然而,成年期肠道微生物群的改变与食物过敏之间的关系尚不清楚。(2)方法:我们建立了三个小鼠模型来分析肠道微生物群失调对肠道屏障的影响,并确定这种影响是否会增加以后生活中食物过敏的易感性和严重程度。(3)结果:抗生素诱导的肠道微生物群失调显著减少了lachnospiraceae、muribaculaceae 和 ruminococcaceae,增加了 enterococcaceae 和 clostridiales。同时,代谢丰度发生了变化,包括短链脂肪酸和色氨酸减少,嘌呤增加。这种变化与食物过敏有关。在肠道微生物群失调后,我们使小鼠致敏。小鼠血清中特异性 IgE 和 IgG1 的含量显著增加,炎症反应增强。肠道微生物群的失调使致敏小鼠在再次暴露于过敏原时出现更严重的过敏症状、绒毛破裂和紧密连接蛋白(TJs)减少。(4)结论:抗生素诱导的肠道微生物群失调增加了食物过敏的易感性和严重程度。这一事件可能是由于肠道紧密连接蛋白减少导致的肠道通透性增加和炎症反应增强所致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/b63bd01be96e/nutrients-13-03315-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/eb6bbb950c1f/nutrients-13-03315-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/bff034ee94c3/nutrients-13-03315-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/df763d3d6d73/nutrients-13-03315-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/7da4039f57b5/nutrients-13-03315-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/ea77398ba136/nutrients-13-03315-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/d742b9503282/nutrients-13-03315-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/0a424d2c704a/nutrients-13-03315-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/c64415052878/nutrients-13-03315-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/72d46a7166ad/nutrients-13-03315-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/b63bd01be96e/nutrients-13-03315-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/eb6bbb950c1f/nutrients-13-03315-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/bff034ee94c3/nutrients-13-03315-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/df763d3d6d73/nutrients-13-03315-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/7da4039f57b5/nutrients-13-03315-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/ea77398ba136/nutrients-13-03315-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/d742b9503282/nutrients-13-03315-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/0a424d2c704a/nutrients-13-03315-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/c64415052878/nutrients-13-03315-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/72d46a7166ad/nutrients-13-03315-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c371/8539551/b63bd01be96e/nutrients-13-03315-g010.jpg

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本文引用的文献

[1]
Gut microbiome, endocrine control of gut barrier function and metabolic diseases.

J Endocrinol. 2021-2

[2]
Apigenin Attenuates the Allergic Reactions by Competitively Binding to ER With Estradiol.

Front Pharmacol. 2020-7-16

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Dysregulation of intestinal epithelial CFTR-dependent Cl ion transport and paracellular barrier function drives gastrointestinal symptoms of food-induced anaphylaxis in mice.

Mucosal Immunol. 2021-1

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High dietary fat intake induces a microbiota signature that promotes food allergy.

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