全球范围内,估计有1.07亿人患有酒精使用障碍(AUD),每年导致280万人过早死亡。结核病(TB)是全球主要的死亡原因之一,估计全球超过8%的结核病病例归因于AUD。健康的社会决定因素,例如贫困和营养不良,通常在AUD和TB患者中共享,可以解释它们之间的流行病学关联。然而,最近的研究表明,这些共同的风险因素并不能完全解释AUD患者的结核病风险增加.事实上,AUD已被证明是结核病的独立危险因素,随着饮酒的增加,结核病的风险呈线性增加。虽然很少有研究关注AUD和TB之间潜在的生物学机制,酒精对肺部免疫的影响与结核分枝杆菌(Mtb)建立感染的机制之间存在大量重叠。酒精滥用会损害肺泡巨噬细胞的免疫功能,肺固有的先天免疫效应和下呼吸道抗Mtb的第一道防线。长期饮酒也会增加肺泡腔的氧化应激,这反过来可以促进Mtb的增长。在这份手稿中,我们回顾了将AUD与TB联系起来的流行病学数据.我们讨论了有关酒精增加结核病风险的潜在机制的现有文献,并回顾了酒精摄入对肺免疫的已知影响,以阐明Mtb可能利用的其他机制。对AUD和TB之间的联系的更深入了解将促进双重疾病干预和宿主导向疗法的发展,以改善肺部健康和TB的长期结果。
Globally, an estimated 107 million people have an alcohol use disorder (AUD) leading to 2.8 million premature deaths each year. Tuberculosis (TB) is one of the leading causes of death globally and over 8% of global TB cases are estimated to be attributable to AUD. Social determinants of health such as poverty and undernutrition are often shared among those with AUD and TB and could explain the epidemiologic association between them. However, recent studies suggest that these shared risk factors do not fully account for the increased risk of TB in people with AUD. In fact, AUD has been shown to be an independent risk factor for TB, with a linear increase in the risk for TB with increasing alcohol consumption. While few studies have focused on potential biological mechanisms underlying the link between AUD and TB, substantial overlap exists between the effects of alcohol on lung immunity and the mechanisms exploited by Mycobacterium tuberculosis (Mtb) to establish infection. Alcohol misuse impairs the immune functions of the alveolar macrophage, the resident innate immune effector in the lung and the first line of defense against Mtb in the lower respiratory tract. Chronic alcohol ingestion also increases oxidative stress in the alveolar space, which could in turn facilitate Mtb growth. In this manuscript, we
review the epidemiologic data that links AUD to TB. We discuss the existing literature on the potential mechanisms by which alcohol increases the risk of TB and
review the known effects of alcohol ingestion on lung immunity to elucidate other mechanisms that Mtb may exploit. A more in-depth understanding of the link between AUD and TB will facilitate the development of dual-disease interventions and host-directed therapies to improve lung health and long-term outcomes of TB.