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Macrophage lipid body induction by Chagas disease in vivo: putative intracellular domains for eicosanoid formation during infection.

机译:南美锥虫病体内巨噬细胞脂质体诱导:感染过程中类花生酸形成的推测细胞内结构域。

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摘要

Lipid bodies (LB), lipid-rich inclusions abundantly present in cells engaged in inflammation, are specialized intracellular domains involved in generating inflammatory mediators, the eicosanoids. Since the acute Trypanosoma cruzi infection triggers a potent inflammatory reaction characterized by a great increase of peripheral blood monocyte (PBM) and macrophage numbers, we investigated the LB occurrence in these cells. The experimental rat infection by T. cruzi (Y strain) induced significant increase of the LB numbers in peritoneal macrophages at day 6 and 12, accompanied by significant enhancement of Prostaglandin E(2) (PGE(2)) production, as measured by EIA. At day 12, ultrastructural analysis of the heart, a target organ of the disease, showed numerous macrophages with LB prominently increased in number (mean of 8.3 per section view, range of 1-25) compared to controls (mean of 2.6 per section view, range of 0-3) and size. PBM from all groups rarely showed LB. Our results demonstrate, for the first time, that T. cruzi infection in rats elicits important LB formation in inflammatory macrophages but not in PBM. The increase in LB numbers during infection positively correlates with increased generation of PGE(2), suggesting that LB may have a role in the heightened eicosanoid production observed during T. cruzi infection.
机译:脂质体(LB)是参与炎症的细胞中大量存在的富含脂质的包裹体,是专门的细胞内结构域,参与产生炎症介质类二十烷酸。由于急性克鲁氏锥虫感染会引发强烈的炎症反应,其特征是外周血单核细胞(PBM)和巨噬细胞数量大量增加,因此我们调查了这些细胞中LB的发生。实验鼠感染克鲁维氏酵母(Y株)在第6天和第12天导致腹膜巨噬细胞中LB数量显着增加,同时前列腺素E(2)(PGE(2))的产生显着增强,如EIA所测量。在第12天,对心脏(疾病的目标器官)的超微结构分析显示,与对照组相比,LB的巨噬细胞数量显着增加(平均每节视图8.3,每范围1-25),而LB显着增加(平均每节视图2.6) ,范围为0-3)和尺寸。所有组的PBM很少显示LB。我们的研究结果首次证明,大鼠的克氏锥虫感染在炎性巨噬细胞中引起了重要的LB形成,而在PBM中却没有。感染期间LB数量的增加与PGE生成的增加呈正相关(2),这表明LB可能在克鲁氏锥虫感染期间观察到的类花生酸产量增加中起作用。

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