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首页> 外文学位 >Macrophage and bone marrow derived monocyte activation during mouse lung tumorigenesis and chronic inflammation.
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Macrophage and bone marrow derived monocyte activation during mouse lung tumorigenesis and chronic inflammation.

机译：小鼠肺肿瘤发生和慢性炎症过程中巨噬细胞和骨髓衍生的单核细胞活化。

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The link between inflammation and cancer has been known since Virchow first described leukocytes near human tumors. Recently, the power of inflammatory cells as promoting factors in tumor development has been more thoroughly explored. I examined the activation state of tumor associated macrophages (TAMS) during chemically induced pulmonary carcinogenesis. Alternative/M2 macrophage activation characterized by high arginase I, and classical/MI activation (high inducible nitric oxide synthase (iNOS)) were determined in several cancer models. The activation phenotype of bone marrow derived monocytes (BDMCs) infiltrating tumor-bearing organs mirrors that of TAMs and begins after local activation. While activation varies depending on genetic background, mode of tumor induction, and stage of progression, M2 activation predominates when tumors are present. The number of resident macrophages and degree of BDMC infiltration into lungs depends upon strain and is not influenced by activation state, indicating separate mechanisms for infiltration and activation.;Macrophages not only influence tumor development, but can influence cytokine and prostaglandin (PG) production from neighboring cells. Co-culture of an alveolar macrophage cell line (MH-S) decreased both PGE2 and PGI 2 production from primary bronchiolar Clara cells from naive and tumor-bearing mice, as well as altering inflammatory cytokines IL-6, IL-12, and IL-10.;Alternative activation of macrophages is not only associated with tumors. Inflammation induced by butylated hydroxytoluene (BHT) or Mycobacterium tuberculosis initially activates pulmonary macrophages to M1 and then to M2 during chronic inflammation. While tumors and BHT influence bone marrow macrophage populations, BDMCs are not altered upon infection with M. tuberculosis.;Macrophage activation is due to exposure to specific cytokines. IFN-gamma induces M1 activation, while IL-4 and IL-13 induce M2 activation. Macrophages and BMDCs from IFN-gamma KO mice do not become classically activated, allowing tumors to grow 1.3-fold larger than wild type mice. Genetic ablation of IL-4Ralpha, the receptor for both IL-4 and IL-13, prevents alternative activation of TAMs and BDMCs and reduces tumor size 1.3-fold compared to wild type mice. Defining the dynamic tumor-macrophage dialogue during chronic inflammation may lead to novel diagnostic and therapeutic strategies.
机译：自Virchow首次描述人类肿瘤附近的白细胞以来，就已经知道炎症和癌症之间的联系。最近，炎症细胞作为肿瘤发展促进因子的作用已得到更彻底的探索。我检查了化学诱导的肺致癌过程中肿瘤相关巨噬细胞（TAMS）的激活状态。在几种癌症模型中确定了以高精氨酸酶I为特征的替代性/ M2巨噬细胞活化和经典/ MI活化（高诱导型一氧化氮合酶（iNOS））。浸润荷瘤器官的骨髓衍生单核细胞（BDMC）的激活表型与TAM相似，并在局部激活后开始。虽然激活取决于遗传背景，肿瘤诱导方式和进展阶段，但存在肿瘤时，M2激活占主导地位。驻留巨噬细胞的数量和BDMC浸入肺的程度取决于菌株，不受激活状态的影响，表明浸润和激活的机制不同。巨噬细胞不仅影响肿瘤的发生，而且可以影响细胞因子和前列腺素（PG）的产生相邻细胞。肺泡巨噬细胞系（MH-S）的共培养减少了来自幼稚和荷瘤小鼠的初级细支气管Clara细胞的PGE2和PGI 2产生，并改变了炎性细胞因子IL-6，IL-12和IL -10 .；巨噬细胞的替代激活不仅与肿瘤有关。丁基化羟基甲苯（BHT）或结核分枝杆菌引起的炎症最初在慢性炎症期间将肺巨噬细胞激活为M1，然后激活为M2。尽管肿瘤和BHT影响了骨髓巨噬细胞的数量，但在感染结核分枝杆菌后BDMC并没有改变。巨噬细胞的活化是由于暴露于特定的细胞因子引起的。 IFN-γ诱导M1激活，而IL-4和IL-13诱导M2激活。 IFN-γKO小鼠的巨噬细胞和BMDC并未被经典激活，从而使肿瘤的生长比野生型小鼠大1.3倍。与野生型小鼠相比，IL-4Ralpha（IL-4和IL-13的受体）的遗传消融可防止TAM和BDMC的交替激活，并使肿瘤大小减小1.3倍。在慢性炎症期间定义动态的肿瘤-巨噬细胞对话可能会导致新的诊断和治疗策略。

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