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首页> 外文期刊>Journal of immunotherapy >Augmented macrophage differentiation and polarization of tumor-associated macrophages towards m1 subtype in listeria-administered tumor-bearing host
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Augmented macrophage differentiation and polarization of tumor-associated macrophages towards m1 subtype in listeria-administered tumor-bearing host

机译：李斯特菌所致荷瘤宿主中肿瘤相关巨噬细胞向m1亚型的增强巨噬细胞分化和极化

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This study investigates the effect of Listeria administration on differentiation of macrophages from precursor bone marrow cells and functional status of tumor-associated macrophages (TAM). Listeria administration not only resulted in an augmented infiltration of tumor by F4/80 macrophages but also repolarized the functional status of TAM displaying features of some M1 macrophage subtype with upregulated phagocytosis and tumoricidal activity accompanied by altered expression of monocarboxylate transporter-1, toll-like receptor-2, surface markers: CD11c, interleukin-2 receptor, CD62L, and secreted molecules: nitric oxide, interleukin (IL)-1, IL-6, tumor necrosis factor-α, and vascular endothelial growth factor. Declined tumor cell survival and modulated repertoire of cytokines: interferon-γ, IL-6, IL-10, and transforming growth factor-β in tumor microenvironment indicated their role in polarization of TAM towards proinflammatory state. Bone marrow cell of Listeria-administered tumor-bearing mice showed augmented survival, declined expression of p53 upregulated modulator of apoptosis with an upregulated differentiation into activation responsive bone marrow-derived macrophages along with altered expression of macrophage-colony stimulating factor, macrophage-colony stimulating factor receptor, and granulocyte macrophage-colony stimulating factor receptor. These findings indicate that Listeria infection is associated with an augmented differentiation of macrophages accompanied by tumoricidal activation of TAM.
机译：这项研究调查了李斯特菌对巨噬细胞从前体骨髓细胞分化和肿瘤相关巨噬细胞（TAM）的功能状态的影响。李斯特菌的施用不仅导致F4 / 80巨噬细胞对肿瘤的浸润增加，而且使TAM的功能状态重新极化，显示某些M1巨噬细胞亚型的特征，吞噬作用和杀虫活性上调，并伴有单羧酸盐转运蛋白1表达的改变，类似收费。受体2，表面标志物：CD11c，白介素2受体，CD62L和分泌的分子：一氧化氮，白介素（IL）-1，IL-6，肿瘤坏死因子-α和血管内皮生长因子。肿瘤微环境中肿瘤细胞存活率下降和细胞因子调节谱：干扰素-γ，IL-6，IL-10和转化生长因子-β表明它们在TAM极化向促炎状态中发挥作用。李斯特菌属荷瘤小鼠的骨髓细胞显示出增加的存活力，p53上调的细胞凋亡调节剂表达下降，向活化反应性骨髓来源的巨噬细胞的分化分化以及巨噬细胞集落刺激因子，巨噬细胞集落刺激因子的表达变化受体和粒细胞巨噬细胞集落刺激因子受体。这些发现表明，李斯特菌感染与巨噬细胞的分化增强有关，并伴随着TAM的杀癌活性。

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