Chan Edward D, Kinney William H, Honda Jennifer R, Bishwakarma Raju, Gangavelli Avani, Mya Jenny, Bai Xiyuan, Ordway Diane J
Department of Medicine, Denver Veterans Affairs Medical Center, 1055 Clermont St, Denver, CO 80220, USA; Departments of Medicine and Academic Affairs, D509, Neustadt Building, National Jewish Health, 1400 Jackson St, Denver, CO 80206, USA; Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz Medical Campus, Research 2, Box C-272, 9th Floor, 12700 East 19th Avenue, Aurora, CO 80045, USA.
Departments of Medicine and Academic Affairs, D509, Neustadt Building, National Jewish Health, 1400 Jackson St, Denver, CO 80206, USA.
Tuberculosis (Edinb). 2014 Dec;94(6):544-50. doi: 10.1016/j.tube.2014.08.010. Epub 2014 Sep 28.
In many regions of the world, there is a great overlap between the prevalence of cigarette smoke exposure and tuberculosis. Despite the large body of epidemiologic evidence that tobacco smoke exposure is associated with increased tuberculosis infection, active disease, severity of disease, and mortality from tuberculosis, these studies cannot distinguish whether the mechanism is principally through direct impairment of anti-tuberculosis immunity by cigarette smoke or due to potential confounders that increase risk for tuberculosis and are commonly associated with smoking--such as poverty, malnutrition, and crowded living conditions. While there are several in vivo murine and in vitro macrophage studies showing cigarette smoke impairs control of tuberculous infection, little is known of the molecular and cellular mechanisms by which this impairment occurs. Herein, we highlight the key findings of these studies. Additionally, we review key immune cells that play critical roles in host-defense or pathogenesis of tuberculosis and generate a hypothesis-driven discussion of the possible mechanisms by which cigarette smoke impairs or enhances their functions, respectively, ultimately resulting in compromised immunity against tuberculosis.
在世界许多地区，接触香烟烟雾的人群与结核病患者群体有很大重叠。尽管有大量流行病学证据表明，接触烟草烟雾会增加结核病感染、活动性疾病、疾病严重程度以及结核病死亡率，但这些研究无法区分其机制主要是香烟烟雾直接损害抗结核免疫力，还是由于增加结核病风险且通常与吸烟相关的潜在混杂因素——如贫困、营养不良和拥挤的生活条件。虽然有多项体内小鼠和体外巨噬细胞研究表明香烟烟雾会损害对结核感染的控制，但对于这种损害发生的分子和细胞机制却知之甚少。在此，我们重点介绍这些研究的关键发现。此外，我们回顾了在结核病宿主防御或发病机制中起关键作用的关键免疫细胞，并分别针对香烟烟雾损害或增强其功能的可能机制展开基于假设的讨论，最终导致抗结核免疫力受损。
