Cirrhosis is a multisystemic disease wherein inflammatory responses originating from advanced liver disease and its sequelae affect distant compartments. Patients with cirrhosis are susceptible to bacterial infections, which may precipitate acute decompensation and acute-on-chronic liver failure, both of which are associated with high short-term mortality. Innate immune cells are an essential first line of defence against pathogens. Activation of liver macrophages (Kupffer cells) and resident mastocytes generate proinflammatory and vaso-permeating mediators that induce accumulation of neutrophils, lymphocytes, eosinophils and monocytes in the liver, and promote tissue damage. During cirrhosis progression, damage- and pathogen-associated molecular patterns activate immune cells and promote development of systemic inflammatory responses which may involve different tissues and compartments. The antibacterial function of circulating neutrophils and monocytes is gradually and severely impaired as cirrhosis worsens, contributing to disease progression. The mechanisms underlying impaired antimicrobial responses are complex and incompletely understood. This review focuses on the continuous and distinct perturbations arising in innate immune cells during cirrhosis, including their impact on disease progression, as well as reviewing potential therapeutic targets.

中文翻译：

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肝硬化中的先天免疫细胞


肝硬化是一种多系统疾病，其中源自晚期肝病及其后遗症的炎症反应影响远处的隔室。肝硬化患者容易受到细菌感染，这可能会导致急性失代偿和慢性肝衰竭急性发作，这两者都与高短期死亡率相关。先天免疫细胞是抵御病原体的重要第一道防线。肝脏巨噬细胞（库普弗细胞）和常驻肥大细胞的激活产生促炎和血管渗透介质，诱导中性粒细胞、淋巴细胞、嗜酸性粒细胞和单核细胞在肝脏中积聚，并促进组织损伤。在肝硬化进展过程中，损伤和病原体相关的分子模式激活免疫细胞并促进可能涉及不同组织和区室的全身炎症反应的发展。随着肝硬化恶化，循环中性粒细胞和单核细胞的抗菌功能逐渐严重受损，导致疾病进展。抗菌反应受损的机制很复杂且尚未完全了解。本综述重点关注肝硬化期间先天免疫细胞产生的持续且独特的扰动，包括它们对疾病进展的影响，以及回顾潜在的治疗靶点。