气体递质在结核病发病机制中的新作用。
The emerging role of gasotransmitters in the pathogenesis of tuberculosis.
作者信息
Chinta Krishna C, Saini Vikram, Glasgow Joel N, Mazorodze James H, Rahman Md Aejazur, Reddy Darshan, Lancaster Jack R, Steyn Adrie J C
机构信息
Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL, USA.
Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL, USA; UAB Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL, USA.
出版信息
Nitric Oxide. 2016 Sep 30;59:28-41. doi: 10.1016/j.niox.2016.06.009. Epub 2016 Jul 4.
Mycobacterium tuberculosis (Mtb) is a facultative intracellular pathogen and the second largest contributor to global mortality caused by an infectious agent after HIV. In infected host cells, Mtb is faced with a harsh intracellular environment including hypoxia and the release of nitric oxide (NO) and carbon monoxide (CO) by immune cells. Hypoxia, NO and CO induce a state of in vitro dormancy where Mtb senses these gases via the DosS and DosT heme sensor kinase proteins, which in turn induce a set of ∼47 genes, known as the Mtb Dos dormancy regulon. On the contrary, both iNOS and HO-1, which produce NO and CO, respectively, have been shown to be important against mycobacterial disease progression. In this review, we discuss the impact of O2, NO and CO on Mtb physiology and in host responses to Mtb infection as well as the potential role of another major endogenous gas, hydrogen sulfide (H2S), in Mtb pathogenesis.
结核分枝杆菌（Mtb）是一种兼性细胞内病原体，是继艾滋病毒之后导致全球死亡的第二大传染性病原体。在受感染的宿主细胞中，Mtb面临着恶劣的细胞内环境，包括缺氧以及免疫细胞释放一氧化氮（NO）和一氧化碳（CO）。缺氧、NO和CO会诱导体外休眠状态，在此状态下，Mtb通过DosS和DosT血红素传感器激酶蛋白感知这些气体，进而诱导一组约47个基因，即所谓的Mtb Dos休眠调节子。相反，分别产生NO和CO的诱导型一氧化氮合酶（iNOS）和血红素加氧酶-1（HO-1）均已被证明对分枝杆菌疾病进展具有重要作用。在本综述中，我们讨论了氧气、NO和CO对Mtb生理学以及宿主对Mtb感染反应的影响，以及另一种主要内源性气体硫化氢（H2S）在Mtb发病机制中的潜在作用。
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