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Thinking bigger: How early-life environmental exposures shape the gut microbiome and influence the development of asthma and allergic disease

期刊

ALLERGY
卷 74, 期 11, 页码 2103-2115

出版社

WILEY
DOI: 10.1111/all.13812

关键词

omics and systems biology; asthma; basic mechanisms; environment and hygiene hypothesis; microbiome; personalized medicine

资金

  1. Canadian Institutes Health Research Funding Source: Medline
  2. Genome Canada [274CHI] Funding Source: Medline
  3. Michael Smith Foundation for Health Research Funding Source: Medline
  4. Genome BC Funding Source: Medline
  5. AllerGen NCE Funding Source: Medline

向作者/读者索取更多资源

Imbalance, or dysbiosis, of the gut microbiome of infants has been linked to an increased risk of asthma and allergic diseases. Most studies to date have provided a wealth of data showing correlations between early-life risk factors for disease and changes in the structure of the gut microbiome that disrupt normal immunoregulation. These studies have typically focused on one specific risk factor, such as mode of delivery or early-life antibiotic use. Such micro-level exposures have a considerable impact on affected individuals but not necessarily the whole population. In this review, we place these mechanisms under a larger lens that takes into account the influence of upstream macro-level environmental factors such as air pollution and the built environment. While these exposures likely have a smaller impact on the microbiome at an individual level, their ubiquitous nature confers them with a large influence at the population level. We focus on features of the indoor and outdoor human-made environment, their microbiomes and the research challenges inherent in integrating the built environment microbiomes with the early-life gut microbiome. We argue that an exposome perspective integrating internal and external microbiomes with macro-level environmental factors can provide a more comprehensive framework to define how environmental exposures can shape the gut microbiome and influence the development of allergic disease.

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