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Gut microbiome in the first 1000 days and risk for childhood food allergy

微生物群 免疫学 生物 食物过敏 失调 怀孕 疾病 肠道菌群 过敏 医学 生物信息学 遗传学 内科学
作者
Ethan Davis,Cynthia Johnson,Richard A. Insel,Kirsi M. Järvinen
出处
期刊:Annals of Allergy Asthma & Immunology [Elsevier]
卷期号:133 (3): 252-261 被引量:3
标识
DOI:10.1016/j.anai.2024.03.010
摘要

Objective To summarize recent data on the association between gut microbiome composition and food allergy (FA) in early childhood and highlight potential host-microbiome interactions that reinforce or abrogate oral tolerance. Data sources PubMed search of English-language articles related to FA, other atopic disease, and the gut microbiome in pregnancy and early childhood. Study selections Human studies published after 2015 assessing the relationship between the gut bacteriome and virome in the first 2 years of life and FA or FS development in early childhood were prioritized. Additional human studies conducted on the prenatal gut microbiome or other atopic diseases as well as preclinical studies are also discussed. Results Children who developed FA harbored lower abundances of Bifidobacterium and Clostridia species and had a less mature microbiome during infancy. The early bacterial microbiome protects against FA through production of anti-inflammatory metabolites and induction of T regulatory cells and may also affect FA risk through a role in trained immunity. Infant enteric phage communities are related to childhood asthma development, though no data are available for FA. Maternal gut microbiome during pregnancy is associated with childhood FA risk, potentially via transplacental delivery of maternal bacterial metabolites, though human studies are lacking. Conclusion The maternal and infant microbiomes throughout the first 1000 days of life influence FA risk through a number of proposed mechanisms. Further large, longitudinal cohort studies employing taxonomic, functional, and metabolomic analysis of the bacterial and viral microbiomes are needed to provide further insight on the host-microbe interactions underlying FA pathogenesis in childhood.
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