Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis, which is transmitted via aerosol. TB is a secular fatal disease which still represents a health problem worldwide. TB has long incubation period and usually at first, affects the lungs. However, the infection could also attack other organs including lymph nodes, abdomen, genitourinary tract, skin, joints, bones and nervous system, what are known as extrapulmonary TB (EPTB). The granulomatous lesions are characterized by necrosis and liquefaction, which causes several lungs damages. Granulomas have traditionally been known to be protective host structures, but mycobacteria can use granuloma as vehicle for expansion by intercellular spread, and it might facilitate M. tuberculosis dissemination to other body areas. Hypoxia, which occurs in granuloma areas contribute to disease progression, as the bacilli adapt to lack of oxygen and low nutrient concentration leading to modulation of angiogenesis genes expression. Induction of angiogenesis has controversial actions, while it could benefit the host by providing a direct source for the arrival of immune system cells against a pathogen, this conditions can also promote bacterial growth and spread to other tissues. This occurs due a greater supply of oxygen and nutrients. Epigenetic processes, such as miRNAs fluctuations, modulate angiogenesis resulting in pathogen mediated interference in angiogenic processes. M. tuberculosis infection affects microRNA expression profile in host tissues. Several miRNAs are involved in cell development, proliferation, differentiation, apoptosis, and even anti-inflammatory and pro-inflammatory stimuli. MicroRNAs promote dual role on M. tuberculosis infection, persistence, and host immune system modulation. These molecules might represent great potential as biomarkers of disease progression, spread, activity, and latency. The purpose of this review is to discuss how epigenetic mechanisms can influence the spread of Mycobacterium tuberculosis, affecting the expression of mediators of angiogenesis, the formation of granuloma, and the installation of the disease.

中文翻译：

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结核病：一种由表观遗传因素介导的肉芽肿性疾病

结核病 (TB) 是由结核分枝杆菌引起的传染病，通过气溶胶传播。结核病是一种长期致命的疾病，仍然是世界范围内的健康问题。结核病潜伏期很长，通常首先会影响肺部。然而，感染也可能侵袭其他器官，包括淋巴结、腹部、泌尿生殖道、皮肤、关节、骨骼和神经系统，即所谓的肺外结核病 (EPTB)。肉芽肿性病变的特点是坏死和液化，这会导致一些肺部损伤。肉芽肿传统上被认为是保护性宿主结构，但分枝杆菌可以使用肉芽肿作为通过细胞间传播进行扩张的载体，并且它可能促进结核分枝杆菌传播到其他身体部位。缺氧，这发生在肉芽肿区域有助于疾病进展，因为杆菌适应缺氧和低营养浓度导致血管生成基因表达的调节。诱导血管生成具有有争议的作用，虽然它可以通过为免疫系统细胞到达对抗病原体提供直接来源而使宿主受益，但这种情况也可以促进细菌生长并扩散到其他组织。这是由于更多的氧气和营养供应。表观遗传过程，例如 miRNA 的波动，调节血管生成，导致病原体介导的对血管生成过程的干扰。结核分枝杆菌感染影响宿主组织中的 microRNA 表达谱。几种 miRNA 参与细胞发育、增殖、分化、凋亡、甚至抗炎和促炎刺激。MicroRNA 促进对结核分枝杆菌感染、持久性和宿主免疫系统调节的双重作用。这些分子可能代表着作为疾病进展、传播、活动和潜伏期的生物标志物的巨大潜力。本综述的目的是讨论表观遗传机制如何影响结核分枝杆菌的传播、影响血管生成介质的表达、肉芽肿的形成和疾病的发生。