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结核分枝杆菌 PPE2 蛋白可能抑制活化巨噬细胞中的一氧化氮。

PPE2 protein of Mycobacterium tuberculosis may inhibit nitric oxide in activated macrophages.

机构信息

Centre for DNA Fingerprinting and Diagnostics, Nampally, Andhra Pradesh, India.

出版信息

Ann N Y Acad Sci. 2013 Apr;1283:97-101. doi: 10.1111/nyas.12070. Epub 2013 Feb 28.

DOI:10.1111/nyas.12070
PMID:23448669
Abstract

Although the pathophysiological role of PE/PPE proteins of Mycobacterium tuberculosis is yet to be fully understood, recent evidence shows that these proteins play important roles in antigenic diversity, as well as in host-pathogen interactions and mycobacterial pathogenesis. Most of the PE/PPE proteins are highly expressed in pathogenic bacteria, pointing to their role in the pathogenesis of mycobacteria. Here, we provide an overview of our work in progress on a specific PPE protein, PPE2 (Rv0256c), which may inhibit nitric oxide (NO) production in activated macrophages. As NO and its by-products are considered to be toxic to bacilli, it is possible that the bacilli recruit Rv0256c in order to inhibit higher production of NO during infection.

摘要

虽然结核分枝杆菌的 PE/PPE 蛋白的病理生理作用尚未完全了解,但最近的证据表明,这些蛋白在抗原多样性以及宿主-病原体相互作用和分枝杆菌发病机制中发挥重要作用。大多数 PE/PPE 蛋白在致病性细菌中高度表达,这表明它们在分枝杆菌的发病机制中发挥作用。在这里,我们概述了我们正在进行的一项关于特定 PPE 蛋白 PPE2(Rv0256c)的工作,该蛋白可能抑制激活的巨噬细胞中一氧化氮(NO)的产生。由于 NO 及其副产物被认为对杆菌有毒,因此杆菌可能招募 Rv0256c 以抑制感染过程中 NO 的更高产生。

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