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Gut Microbiota and Allergic Disease. New Insights

机译:肠道菌群和过敏性疾病。新见解

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摘要

The rapid rise in childhood allergies (atopy) in Westernized nations has implicated associated environmental exposures and lifestyles as primary drivers of disease development. Culture-based microbiological studies indicate that atopy has demonstrable ties to altered gut microbial colonization in very early life. Infants who exhibit more severe multisensitization to food- or aero-allergens have a significantly higher risk of subsequently developing asthma in childhood. Hence an emerging hypothesis posits that environment- or lifestyle-driven aberrancies in the early-life gut microbiome composition and by extension, microbial function, represent a key mediator of childhood allergic asthma. Animal studies support this hypothesis. Environmental microbial exposures epidemiologically associated with allergy protection in humans confer protection against airway allergy in mice. In addition, gut microbiome–derived short-chain fatty acids produced from a high-fiber diet have been shown to protect against allergy via modulation of both local and remote mucosal immunity as well as hematopoietic antigen-presenting cell populations. Here we review key data supporting the concept of a gut–airway axis and its critical role in childhood atopy.
机译:在西方国家,儿童过敏症(儿童型)的迅速增加已将相关的环境暴露和生活方式作为疾病发展的主要驱动力。基于文化的微生物学研究表明,特应性与非常早的肠道微生物定植改变有着明显的联系。对食物或空气过敏原表现出更为严重的多敏性的婴儿,其在儿童期随后患上哮喘的风险明显更高。因此,一个新的假说认为,环境或生活方式驱动的畸形在早期肠道微生物组的组成以及微生物功能的扩展是儿童过敏性哮喘的关键介质。动物研究支持这一假设。流行病学上与人类过敏保护相关的环境微生物暴露赋予小鼠抗气道过敏的保护作用。此外,高纤维饮食产生的源自肠道微生物的短链脂肪酸已显示可通过调节局部和远端粘膜免疫以及造血抗原呈递细胞群来防止过敏。在这里,我们回顾支持肠气道轴概念及其在儿童特应性中的关键作用的关键数据。

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