Maternal antibiotics augment hyperoxia-induced lung injury in neonatal mice.
Maternal antibiotics augment hyperoxia-induced lung injury in neonatal mice.
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母体抗生素会加重新生小鼠高氧诱导的肺损伤。
DOI：
10.1152/ajplung.00442.2019
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发表时间：
2020
期刊：
影响因子：
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通讯作者：
Ambalavanan,Namasivayam
中科院分区：
文献类型：
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作者：
Lal,CharitharthVivek;Ambalavanan,Namasivayam
更快、更便宜的下一代测序技术的出现迅速扩大了我们对微生物组对人类健康影响的理解。现在已经确定的是，人类拥有数十亿的浮游生物。这些微生物不仅在肠道、皮肤和口咽中形成不同的10个群落（1），而且如其他人（3）11和我们的小组（4，5）所述，存在于气道中。然而，12微生物群中的绝大多数都包含在肠道内，这些微生物对宿主，特别是对免疫系统产生至关重要的发育影响。14免疫系统的成熟和早期肺部发育发生在婴儿早期，当肠道微生物组建立时，这使得研究人员探索16肠道微生物组是否有能力影响肺部疾病-一种现在被称为肠-肺轴的现象（6）。围产期抗生素暴露已被证明会加剧过敏性哮喘。Russell等人(8)表明卵清蛋白-19激发的小鼠围产期抗生素暴露通过减少结肠中调节性T细胞积累和增加免疫球蛋白E而加剧气道炎症。在进一步的工作中，这组研究人员将人类肠道微生物组中的21种生态失调变化联系起来，其特征是四种细菌22属（毛螺菌属，韦荣氏球菌属，粪杆菌属和罗氏菌属）的减少，增加了23种哮喘的风险（1）。他们在他们的小鼠模型中证实，这些分类群的减少与肺部炎症增加相关，而补充剂减少了气道炎症（1）。类似地，在新生小鼠肺炎模型中，Deshmukh et al. (2)26能够表明围产期抗生素暴露导致肠道微生物群改变，27
7 The advent of faster and cheaper next generation sequencing has rapidly expanded our 8 understanding of the impact of the microbiome on human health. It is now well established that 9 humans host many billions of commensal organisms. These microbial organisms form distinct 10 communities not only within the gut and on the skin and in the oropharynx (1), but as others (3) 11 and our group (4, 5) have described, are present in the airways. However, the vast majority of the 12 microbiota is contained within the gut and these organisms exert crucial developmental 13 influences on the host, in particular on the immune system (7). 14 The maturation of the immune system and early pulmonary development occur early in 15 infancy when the gut microbiome becomes established, and this has led investigators to explore 16 if the gut microbiome has the capacity to influence pulmonary disease–a phenomena now 17 termed the gut-lung axis (6). Perinatal antimicrobial exposure has been shown to exacerbate 18 allergic asthma. Russell et al.(8) showed that perinatal antibiotic exposure in ovalbumin–19 challenged mice exacerbated airway inflammation by decreasing regulatory T cell accumulation 20 in the colon and increasing immunoglobulin E. In further work, this group of investigators linked 21 dysbiotic changes in the human gut microbiome characterized by reductions in four bacterial 22 genera (Lachnospira, Veillonella, Faecalibacterium, and Rothia) with an increased risk to 23 develop asthma (1). They confirmed in their mouse model that reductions in these taxa were 24 associated with increased lung inflammation while supplementation reduced airway 25 inflammation (1). Similarly, in a neonatal mouse model of pneumonia, Deshmukh et al.(2) were 26 able to show that perinatal antimicrobial exposure produced alterations in the gut microbiota, 27