Singanayagam Aran, Ritchie Andrew I, Johnston Sebastian L
Airway Disease Infection Section, National Heart and Lung Institute, Imperial College, London, UK.
Curr Opin Pulm Med. 2017 Jan;23(1):41-47. doi: 10.1097/MCP.0000000000000333.
The emergence of next-generation 16S rRNA sequencing techniques has facilitated a more detailed study of the body's microbiota and led to renewed interest in the association between microbial exposure and asthma inception. In this review, we evaluate the evidence that the respiratory tract and intestinal microbiota contribute to asthma pathogenesis and progression.
Human studies have revealed associations between the presence of potentially pathogenic bacteria in the respiratory tract in early life and subsequent risk of allergic sensitization and asthma. Similarly, alterations in the intestinal microbiota of neonates have also been shown to precede the development of asthma. Emerging evidence suggests that the lung microbiota is dysregulated in asthma with specific changes in bacterial diversity and community composition according to severity and phenotype. Studies using germ-free mice have been invaluable in moving our understanding from correlation to causation by demonstrating a mechanistic link between the neonatal microbiota and the development of allergic airway inflammation.
An expanding body of literature supports the hypothesis that early life microbial exposures and bacterial communities within the lung and/or intestine play an important role in shaping early immunological development. Perturbations in the microbiota may promote immune defects associated with the development of asthma and allergic sensitization.
新一代16S rRNA测序技术的出现促进了对人体微生物群更详细的研究,并重新引发了人们对微生物暴露与哮喘发病之间关联的兴趣。在本综述中,我们评估呼吸道和肠道微生物群促成哮喘发病机制及进展的证据。
人体研究揭示了生命早期呼吸道中潜在病原菌的存在与随后发生过敏致敏和哮喘的风险之间的关联。同样,新生儿肠道微生物群的改变也已被证明先于哮喘的发生。新出现的证据表明,哮喘患者的肺部微生物群失调,根据严重程度和表型,细菌多样性和群落组成会发生特定变化。使用无菌小鼠的研究通过证明新生儿微生物群与过敏性气道炎症发展之间的机制联系,在将我们的理解从相关性推进到因果关系方面发挥了重要作用。
越来越多的文献支持这样一种假设,即生命早期的微生物暴露以及肺和/或肠道内的细菌群落对早期免疫发育的形成起着重要作用。微生物群的扰动可能会促进与哮喘发展和过敏致敏相关的免疫缺陷。