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Dual RNA-Seq of Mtb-Infected Macrophages In Vivo Reveals Ontologically Distinct Host-Pathogen Interactions.
Cell Reports ( IF 8.8 ) Pub Date : 2020-01-14 , DOI: 10.1016/j.celrep.2019.12.033
Davide Pisu 1 , Lu Huang 1 , Jennifer K Grenier 2 , David G Russell 1
Affiliation  

Dissecting the in vivo host-pathogen interplay is crucial to understanding the molecular mechanisms governing control or progression of intracellular infections. In this work, we explore the in vivo molecular dynamics of Mtb infection by performing dual RNA-seq on Mycobacterium tuberculosis-infected, ontogenetically distinct macrophage lineages isolated directly from murine lungs. We first define an in vivo signature of 180 genes specifically upregulated by Mtb in mouse lung macrophages, then we uncover a divergent transcriptional response of the bacteria between alveolar macrophages that appear to sustain Mtb growth through increased access to iron and fatty acids and interstitial macrophages that restrict Mtb growth through iron sequestration and higher levels of nitric oxide. We use an enrichment protocol for bacterial transcripts, which enables us to probe Mtb physiology at the host cell level in an in vivo environment, with broader application in understanding the infection dynamics of intracellular pathogens in general.

中文翻译:

体内受Mtb感染的巨噬细胞的双重RNA序列揭示了本体上不同的宿主-病原体相互作用。

剖析体内宿主与病原体之间的相互作用对于理解控制细胞内感染的控制或进展的分子机制至关重要。在这项工作中,我们通过对结核分枝杆菌感染的,从个体肺中直接分离的个体发育不同的巨噬细胞谱系进行双重RNA-seq探索,探索了Mtb感染的体内分子动力学。我们首先定义了在小鼠肺巨噬细胞中由Mtb特异上调的180个基因的体内特征,然后我们揭示了肺泡巨噬细胞之间细菌的不同转录反应,这些肺泡巨噬细胞似乎通过增加对铁和脂肪酸以及间质巨噬细胞的访问来维持Mtb的生长。通过螯合铁和增加一氧化氮水平来限制Mtb的生长。我们对细菌转录本使用富集方案,
更新日期:2020-01-15
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