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Effects of lipopolysaccharide and dexamethasone on the biological characteristics of rats alveolar macrophage

机译:脂多糖和地塞米松对大鼠肺泡巨噬细胞生物学特性的影响

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Alveolar macrophages(AMs) play a central role in lung inflammation and acute lung injury, but also participate actively in the resolution of inflammation after activation. Macrophages (MΦ) represent a dynamic cell population that develops and operates within a changing microenvironment. However, it is not known how the biological characteristic of AM stimulates by lipopolysaccharide (LPS) or desamethasone (DEX) and the relationship between AM and inflammation. In this study, we first observed the morphology in AM isolated from rats differed according to the molecule used. We found that LPS-stimulated AM induced anti-apoptosis and had pro-inflammatory effects; dexamethasone induced AM apoptosis and had anti-inflammatory effects. These results suggested that a balance in macrophage activation, being either stimulated by LPS) or DEX, would be important to participate sequentially in both the induction and the resolution of inflammation. These findings may provide new insight into the lung inflammatory process as well as new fields of investigation for immunotherapy in the fields of acute lung injury/ acute respiratory distress syndrome.
机译:肺泡巨噬细胞(AMs)在肺部炎症和急性肺损伤中起着核心作用,但在激活后也积极参与炎症的消退。巨噬细胞(MΦ)代表动态细胞群体,可以在不断变化的微环境中发育和运行。但是,尚不知道脂多糖(LPS)或地塞米松(DEX)如何刺激AM的生物学特性,以及AM与炎症之间的关系。在这项研究中,我们首先观察到从大鼠中分离出的AM的形态因所使用的分子而异。我们发现,LPS刺激的AM诱导抗凋亡并具有促炎作用。地塞米松诱导AM凋亡并具有抗炎作用。这些结果表明,由LPS或DEX刺激的巨噬细胞活化的平衡对于顺序地参与炎症的诱导和消退是重要的。这些发现可能为急性肺损伤/急性呼吸窘迫综合征领域的肺部炎症过程以及免疫治疗的新研究领域提供新的见解。

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