严重肺炎后的神经紊乱与内源性细菌从肺部转移到大脑有关。

Neurological disorders after severe pneumonia are associated with translocation of endogenous bacteria from the lung to the brain.

机构信息

Laboratory for Biomaterial and Immunoengineering, Institute of Functional Nano & Soft Materials (FUNSOM), Soochow University, Suzhou 215123, China.

Jiangsu Key Laboratory for Biosensors, Institute of Advanced Materials (IAM) and School of Materials Science and Engineering, Nanjing University of Posts & Telecommunications, Nanjing, P. R. China.

出版信息

Sci Adv. 2023 Oct 20;9(42):eadi0699. doi: 10.1126/sciadv.adi0699. Epub 2023 Oct 18.

Abstract

Neurological disorders are a common feature in patients who recover from severe acute pneumonia. However, the underlying mechanisms remain poorly understood. Here, we show that the neurological syndromes after severe acute pneumonia are partly attributed to the translocation of endogenous bacteria from the lung to the brain during pneumonia. Using principal components analysis, similarities were found between the brain's flora species and those of the lungs, indicating that the bacteria detected in the brain may originate from the lungs. We also observed impairment of both the lung-blood and brain-blood barriers, allowing endogenous lung bacteria to invade the brain during pneumonia. An elevated microglia and astrocyte activation signature via bacterial infection-related pathways was observed, indicating a bacterial-induced disruption of brain homeostasis. Collectively, we identify endogenous lung bacteria that play a role in altering brain homeostasis, which provides insight into the mechanism of neurological syndromes after severe pneumonia.

摘要

神经系统疾病是严重急性肺炎患者的常见特征。然而,其潜在机制仍不清楚。在这里,我们表明严重急性肺炎后的神经系统综合征部分归因于肺炎期间内源性细菌从肺部转移到大脑。通过主成分分析,发现大脑菌群与肺部菌群之间存在相似性,表明大脑中检测到的细菌可能来自肺部。我们还观察到肺-血和脑-血屏障的损伤,允许内源性肺细菌在肺炎期间入侵大脑。通过细菌感染相关途径观察到小胶质细胞和星形胶质细胞激活特征的升高,表明细菌诱导的脑内稳态破坏。总的来说,我们确定了在改变脑内稳态中起作用的内源性肺细菌,这为严重肺炎后神经系统综合征的机制提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/066a/10584344/05405ca820c2/sciadv.adi0699-f1.jpg

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