Infant airway microbiota and topical immune perturbations in the origins of childhood asthma
Infant airway microbiota and topical immune perturbations in the origins of childhood asthma
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DOI：
10.1038/s41467-019-12989-7
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发表时间：
2019-11-01
影响因子：
16.6
通讯作者：
Bisgaard, Hans
中科院分区：
文献类型：
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作者：
Thorsen, Jonathan;Rasmussen, Morten A.;Bisgaard, Hans
哮喘被认为是通过生命早期的异常免疫发育而产生的，以响应可能影响气道微生物群的环境暴露。在此，我们通过16 S rRNA基因扩增子测序检查了2010年哥本哈根儿童哮喘前瞻性研究（COPSAC（2010））队列中出生后前三个月的气道微生物群，该队列由700名自出生以来监测哮喘发展的儿童组成。微生物多样性和相对丰度韦荣氏球菌和普雷沃氏菌在一个月大的气道与哮喘的年龄6岁，无论是个人和额外的类群在一个多变量模型。此外，这些细菌的相对丰度较高与气道免疫特征相关，气道免疫特征由TNF-α和IL-1 β降低以及CCL 2和CCL 17增加主导，CCL 2和CCL 17本身是哮喘的独立预测因子。这些发现表明，婴儿早期的微生物群-免疫相互作用机制易患儿童哮喘。
Asthma is believed to arise through early life aberrant immune development in response to environmental exposures that may influence the airway microbiota. Here, we examine the airway microbiota during the first three months of life by 16S rRNA gene amplicon sequencing in the population-based Copenhagen Prospective Studies on Asthma in Child-hood 2010 (COPSAC(2010)) cohort consisting of 700 children monitored for the development of asthma since birth. Microbial diversity and the relative abundances of Veillonella and Prevotella in the airways at age one month are associated with asthma by age 6 years, both individually and with additional taxa in a multivariable model. Higher relative abundance of these bacteria is furthermore associated with an airway immune profile dominated by reduced TNF-alpha and IL-1 beta and increased CCL2 and CCL17, which itself is an independent predictor for asthma. These findings suggest a mechanism of microbiota-immune interactions in early infancy that predisposes to childhood asthma.