中文摘要：
肺微環境控制肺泡巨噬細胞（AMs）的穩態和功能，而AMs是肺免疫的主要調節者，但其潛在機制，尤其是微生物組的作用，尚不清楚。在這里，我們使用Lyz2creEi24fl/fl小鼠，報告了巨噬細胞中EI24缺失會破壞AMs的穩態，但通過代謝重編程增強其吞噬和炎癥反應。因此，Lyz2creEi24fl/fl小鼠在肺部對病毒感染和腫瘤轉移表現出抵抗性。值得注意的是，腸道共生微生物通過TLR2/4信號通路上調AMs中的EI24表達。這些數據表明，微生物群通過上調AMs中的EI24以維持其穩態，但會延緩其在肺中的免疫監視功能。因此，我們的研究表明，刪除EI24可以增強基于巨噬細胞的免疫治療的抗病毒和抗腫瘤效果。
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.
論文信息：
論文題目：Microbiota-induced EI24 improves homeostasis but impedes function of alveolar macrophages via metabolic regulation
期刊名稱：Nature Communications
時間期卷：17, Article number: 2227(2026)
在線時間：2026年1月31日
DOI： doi.org/10.1038/s41467-026-68466-5
產品信息：
貨號：CP-005-005
規格：5ml+5ml
品牌：Liposoma
產地：荷蘭
名稱：Clodronate Liposomes&Controlliposomes氯膦酸鹽脂質體套裝
辦事處：靶點科技
Clodronate Liposomes氯膦酸鹽脂質體在小鼠病毒感染和腫瘤轉移模型清除肺泡巨噬細胞和外周單核巨噬細胞。荷蘭Liposoma巨噬細胞清除劑ClodronateLiposomes見刊于Nature Communications：微生物群誘導的EI24通過代謝調控改善穩態，但阻礙肺泡巨噬細胞功能。
Liposoma巨噬細胞清除劑Clodronate Liposomes氯膦酸二鈉脂質體清除肺泡巨噬細胞和單核巨噬細胞的材料和方法：
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.
材料和方法文獻截圖：
