Neutrophils are commonly recognized as prototypic inflammatory cells: They invade the liver upon injury, have a short half-life in inflamed tissue and aggravate injury as well as inflammatory reactions. This has been conclusively demonstrated for acute acetaminophen injury in mice, where myeloid-cell specific receptor for advanced glycation end products (RAGE)-deficiency dramatically altered neutrophil recruitment to necrotic areas, and high-mobility group box 1 (HMGB1) epithelial cell deficiency in the liver prevented all acetaminophen-induced mortality. This article is protected by copyright. All rights reserved.

中文翻译：

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中性粒细胞通过将 microRNA-223 传递给巨噬细胞来解决肝脏炎症的意外作用

中性粒细胞通常被认为是原型炎症细胞：它们在受伤时侵入肝脏，在发炎组织中的半衰期很短，并且会加重损伤和炎症反应。这已在小鼠急性对乙酰氨基酚损伤中得到最终证明，其中晚期糖基化终产物 (RAGE) 缺乏的髓细胞特异性受体显着改变了坏死区域的中性粒细胞募集，以及高迁移率族框 1 (HMGB1) 上皮细胞缺乏肝脏阻止了所有对乙酰氨基酚引起的死亡。本文受版权保护。版权所有。