Frank Burr Mallory's landmark observation in 1911 on the histopathology of alcoholic liver disease (ALD) was the first identification of a link between inflammation and ALD. In this review, we summarize recent advances regarding the origins and roles of various inflammatory components in ALD. Metabolism of ethanol generates a number of metabolites, including acetate, reactive oxygen species, acetaldehyde, and epigenetic changes, that can induce inflammatory responses. Alcohol and its metabolites can also initiate and aggravate inflammatory conditions by promoting gut leakiness of microbial products, by sensitizing immune cells to stimulation, and by activating innate immune pathways, such as complement. Chronic alcohol consumption also sensitizes nonimmune cells, e.g., hepatocytes, to inflammatory signals and impairs their ability to respond to protective signals. Based on these advances, a number of inflammatory targets have been identified with potential for therapeutic intervention in ALD, presenting new opportunities and challenges for translational research.

中文翻译：

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酒精性肝病中的炎症。

Frank Burr Mallory 在 1911 年对酒精性肝病 (ALD) 组织病理学的里程碑式观察首次确定了炎症与 ALD 之间的联系。在这篇综述中，我们总结了有关 ALD 中各种炎症成分的起源和作用的最新进展。乙醇的代谢会产生许多代谢物，包括醋酸盐、活性氧、乙醛和表观遗传变化，它们可以诱导炎症反应。酒精及其代谢物还可以通过促进微生物产品的肠道渗漏、使免疫细胞对刺激敏感以及激活先天免疫途径（如补体）来引发和加重炎症状况。长期饮酒也会使非免疫细胞敏感，例如肝细胞、炎症信号并削弱它们对保护信号作出反应的能力。基于这些进展，已经确定了许多具有治疗干预 ALD 潜力的炎症靶点，为转化研究带来了新的机遇和挑战。