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Alcohol and lung injury and immunity

机译：酒精和肺损伤和免疫力

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Annually, excessive alcohol use accounts for more than $220 billion in economic costs and 80,000 deaths, making excessive alcohol use the third leading lifestyle-related cause of death in the US. Patients with an alcohol-use disorder (AUD) also have an increased susceptibility to respiratory pathogens and lung injury, including a 2-4-fold increased risk of acute respiratory distress syndrome (ARDS). This review investigates some of the potential mechanisms by which alcohol causes lung injury and impairs lung immunity. In intoxicated individuals with burn injuries, activation of the gut-liver axis drives pulmonary inflammation, thereby negatively impacting morbidity and mortality. In the lung, the upper airway is the first checkpoint to fail in microbe clearance during alcohol-induced lung immune dysfunction. Brief and prolonged alcohol exposure drive different post-translational modifications of novel proteins that control cilia function. Proteomic approaches are needed to identify novel alcohol targets and post-translational modifications in airway cilia that are involved in alcohol-dependent signal transduction pathways. When the upper airway fails to clear inhaled pathogens, they enter the alveolar space where they are primarily cleared by alveolar macrophages (AM). With chronic alcohol ingestion, oxidative stress pathways in the AMs are stimulated, thereby impairing AM immune capacity and pathogen clearance. The epidemiology of pneumococcal pneumonia and AUDs is well established, as both increased predisposition and illness severity have been reported. AUD subjects have increased susceptibility to pneumococcal pneumonia infections, which may be due to the pro-inflammatory response of AMs, leading to increased oxidative stress. (C) 2016 Elsevier Inc. All rights reserved.
机译：每年，过量的酒精使用占经济成本和80,000亿美元以上的220亿美元，使得过度的酒精利用美国的第三个主要的生活方式相关原因。酒精使用障碍（AUD）的患者也对呼吸道病原体和肺损伤的敏感性增加，包括2-4倍的急性呼吸窘迫综合征（ARDS）的风险增加。本综述研究了醇因肺损伤和损害肺免疫力的一些潜在机制。在受烧伤伤害的醉酒中，肠肝轴的激活驱动肺炎症，从而产生了发病率和死亡率。在肺中，上呼吸道是在酒精诱导的肺免疫功能障碍期间在微生物间隙中失效的第一个检查点。简短而长期的酒精暴露驱动控制纤毛功能的新型蛋白质的不同翻译后修饰。需要蛋白质组学方法来识别新的酒精靶标和在含有酒精依赖性信号转导途径的气道纤毛的翻译后修饰。当上呼吸道未能清除吸入病原体时，它们进入肺泡空间，其中它们主要被肺泡巨噬细胞（AM）清除。通过慢性醇摄入，刺激AMS中的氧化应激途径，从而损害AM免疫能力和病原体间隙。由于据报道，肺炎球菌肺炎肺炎肺炎和AUDS的流行病学已经成立了，因此据报道了易感性和疾病严重程度。 AUD受试者对肺炎球菌肺炎感染的敏感性增加，这可能是由于AMS的促炎抗源性，导致氧化应激增加。 （c）2016年Elsevier Inc.保留所有权利。

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