School of Medicine, Tsinghua University, Beijing, People's Republic of China.
Department of Computational and Systems Biology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Thorax. 2021 Dec;76(12):1231-1235. doi: 10.1136/thoraxjnl-2020-216013. Epub 2021 Apr 22.
Host inflammatory responses predict worse outcome in severe pneumonia, yet little is known about what drives dysregulated inflammation. We performed metagenomic sequencing of microbial cell-free DNA (mcfDNA) in 83 mechanically ventilated patients (26 culture-positive, 41 culture-negative pneumonia, 16 uninfected controls). Culture-positive patients had higher levels of mcfDNA than those with culture-negative pneumonia and uninfected controls (p<0.005). Plasma levels of inflammatory biomarkers (fractalkine, procalcitonin, pentraxin-3 and suppression of tumorigenicity-2) were independently associated with mcfDNA levels (adjusted p<0.05) among all patients with pneumonia. Such host-microbe interactions in the systemic circulation of patients with severe pneumonia warrant further large-scale clinical and mechanistic investigations.
宿主炎症反应可预测重症肺炎的不良预后，但尚不清楚是什么导致了失调的炎症。我们对 83 名机械通气患者（26 例培养阳性、41 例培养阴性肺炎、16 例未感染对照）的微生物无细胞 DNA（mcfDNA）进行了宏基因组测序。培养阳性的患者的 mcfDNA 水平高于培养阴性肺炎和未感染对照组（p<0.005）。在所有患有肺炎的患者中，血浆炎症生物标志物（ fractalkine、降钙素原、pentraxin-3 和肿瘤抑制因子-2）水平与 mcfDNA 水平独立相关（调整后的 p<0.05）。严重肺炎患者全身循环中的这种宿主-微生物相互作用值得进一步进行大规模临床和机制研究。
