中文摘要：
肺微环境控制肺泡巨噬细胞（AMs）的稳态和功能，而AMs是肺免疫的主要调节者，但其潜在机制，尤其是微生物组的作用，尚不清楚。在这里，我们使用Lyz2creEi24fl/fl小鼠，报告了巨噬细胞中EI24缺失会破坏AMs的稳态，但通过代谢重编程增强其吞噬和炎症反应。因此，Lyz2creEi24fl/fl小鼠在肺部对病毒感染和肿瘤转移表现出抵抗性。值得注意的是，肠道共生微生物通过TLR2/4信号通路上调AMs中的EI24表达。这些数据表明，微生物群通过上调AMs中的EI24以维持其稳态，但会延缓其在肺中的免疫监视功能。因此，我们的研究表明，删除EI24可以增强基于巨噬细胞的免疫治疗的抗病毒和抗肿瘤效果。
英文摘要：
Lung microenvironment controls the homeostasis and function of alveolar macrophages (AMs), the major regulators of lung immunity, but the underlying mechanisms, particularly the role of microbiota, remain unclear. Here, with Lyz2creEi24fl/fl mice, we report that EI24 deficiency in macrophages disrupts AMs homeostasis but enhances their phagocytosis and inflammatory responses via metabolic rewiring. Consequently, Lyz2creEi24fl/fl mice exhibit resistance to viral infection and tumor metastasis in lung. Notably, EI24 expression in AMs is upregulated by commensal microbiota through TLR2/4 signaling. These data demonstrate that microbiota upregulates EI24 in AMs to favor their homeostasis, but it retards their immune surveillance function in the lung. Our study thus indicates that deleting EI24 enhances anti-viral and anti-tumor effects of macrophage-based immunotherapy.
论文信息：
论文题目：Microbiota-induced EI24 improves homeostasis but impedes function of alveolar macrophages via metabolic regulation
期刊名称：Nature Communications
时间期卷：17, Article number: 2227(2026)
在线时间：2026年1月31日
DOI： doi.org/10.1038/s41467-026-68466-5
产品信息：
货号：CP-005-005
规格：5ml+5ml
品牌：Liposoma
产地：荷兰
名称：Clodronate Liposomes&Controlliposomes氯膦酸盐脂质体套装
办事处：靶点科技
Clodronate Liposomes氯膦酸盐脂质体在小鼠病毒感染和肿瘤转移模型清除肺泡巨噬细胞和外周单核巨噬细胞。荷兰Liposoma巨噬细胞清除剂ClodronateLiposomes见刊于Nature Communications：微生物群诱导的EI24通过代谢调控改善稳态，但阻碍肺泡巨噬细胞功能。
Liposoma巨噬细胞清除剂Clodronate Liposomes氯膦酸二钠脂质体清除肺泡巨噬细胞和单核巨噬细胞的材料和方法：
Mice were first administered i.t. with 100 μL Clodronate or Control liposomes (Liposoma Technology) on day −1 to deplete local AMs, and were subsequently injected i.v. with 100 μL Clodronate or Control liposomes at day 1 and with 5-day intervals to deplete potential monocyte-derived macrophages in lung69. To deplete T cells in vivo, mice were injected i.p. with 200 μg anti-CD4 (clone: GK1.5, Selleck) and 200 μg anti-CD8 (clone: 2.43, Selleck) at 7-day intervals.
材料和方法文献截图：
