Early life stress in mice alters gut microbiota independent of maternal microbiota inheritance
Early life stress in mice alters gut microbiota independent of maternal microbiota inheritance
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DOI：
10.1152/ajpregu.00072.2020
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发表时间：
2021-05-01
影响因子：
2.8
通讯作者：
Pollock, Jennifer S.
中科院分区：
文献类型：
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作者：
Kemp, Keri M.;Colson, Jackson;Pollock, Jennifer S.
暴露于早期生活压力（ELS）与包括抑郁症和心血管疾病在内的慢性疾病发展的更大风险相关。肠道微生物群的改变与小鼠和人类的抑郁症和心血管疾病有关。啮齿动物模型的早期生活忽视的特点之间的机械联系的早期生活压力（ELS）和疾病的风险在以后的生活。然而，人们对ELS暴露和幼鼠肠道微生物群以及肠道微生物群母体遗传的影响知之甚少。我们使用ELS小鼠模型，早期断奶的母体分离（MSEW）和正常饲养的小鼠来确定新生儿微生物群是否发生了变化，如果是这样，则差异可归因于随后传递给后代的母体微生物群的变化。个体扩增子序列变体（ASV）在出生后第28天（PD）与正常饲养的幼崽相比，在MSEW的微生物群中显示出差异丰度。此外，ELS暴露降低了α多样性，并改变了PD28时的微生物群落组成。母体微生物群中个体ASV的组成、α多样性水平和丰度与MSEW或正常饲养的队列相似。因此，观察到的新生儿和幼仔中单个细菌ASV丰度的变化可能是由后代宿主中MSEW的内源性效应驱动的，而不是由于与母体的遗传差异。这些知识表明，暴露于ELS对微生物因素对慢性疾病发展风险有直接影响。
Exposure to early life stress (ELS) is associated with a greater risk of chronic disease development including depression and cardiovascular disease. Altered gut microbiota has been linked to both depression and cardiovascular disease in mice and humans. Rodent models of early life neglect are used to characterize the mechanistic links between early life stress (ELS) and the risk of disease later in life. However, little is understood about ELS exposure and the gut microbiota in the young mice and the influence of the maternal inheritance of the gut microbiota. We used a mouse model of ELS, maternal separation with early weaning (MSEW), and normally reared mice to determine whether the neonate microbiota is altered, and if so, are the differences attributable to changes in dam microbiota that are then transmitted to their offspring. Individual amplicon sequence variants (ASVs) displayed differential abundance in the microbiota of MSEW compared with normally reared pups at postnatal day (PD) 28. Additionally, ELS exposure reduced the alpha diversity and altered microbial community composition at PD28. The composition, levels of alpha diversity, and abundance of individual ASVs in the microbiota of dams were similar from MSEW or normally reared cohorts. Thus, the observed shifts in the abundance of individual bacterial ASVs in the neonates and young pups are likely driven by endogenous effects of MSEW in the offspring host and are not due to inherited differences from the dam. This knowledge suggests that exposure to ELS has a direct effect on microbial factors on the risk of chronic disease development.