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血管紧张素II对曼氏血吸虫病小鼠肉芽肿巨噬细胞吞噬作用和肌动蛋白聚合的刺激作用

Angiotensin II stimulation of granuloma macrophage phagocytosis and actin polymerization in murine schistosomiasis mansoni.

作者信息

Weinstock J V, Kassab J T

出版信息

Cell Immunol. 1984 Nov;89(1):46-54. doi: 10.1016/0008-8749(84)90196-5.

Abstract

In murine schistosomiasis, components of the renin-angiotensin system are present in isolated liver granulomas. Furthermore, granuloma macrophages have receptors for angiotensin II (AII). These observations with other evidence suggest that angiotensins function in immunoregulation. Since AII can stimulate actin-myosin interactions and since macrophages have contractile proteins, it was determined whether AII could alter the phagocytic activity of granuloma macrophages. AII, at concentrations which saturate AII receptors, enhanced phagocytic activity for both unopsonized and opsonized sheep red blood cells (RBC). Using a DNase inhibitory assay, it was also shown that similar concentrations of AII stimulated intracellular actin polymerization. Cytochalasin B, which impedes actin filament interactions, inhibited AII-stimulated phagocytosis. AII analogs, with little-known agonist activity, blocked AII-stimulated actin polymerization and phagocytosis of RBC and RBC opsonized with IgG. These data support the contention that AII binds to AII receptors on the macrophage and stimulates phagocytosis possibly through polymerization of intracellular actin.

摘要

在小鼠血吸虫病中,肾素-血管紧张素系统的成分存在于分离出的肝脏肉芽肿中。此外,肉芽肿巨噬细胞具有血管紧张素II(AII)受体。这些观察结果与其他证据表明血管紧张素在免疫调节中起作用。由于AII能刺激肌动蛋白-肌球蛋白相互作用,且巨噬细胞含有收缩蛋白,因此研究了AII是否会改变肉芽肿巨噬细胞的吞噬活性。饱和AII受体浓度的AII增强了对未调理和调理过的绵羊红细胞(RBC)的吞噬活性。使用DNA酶抑制试验还表明,相似浓度的AII刺激细胞内肌动蛋白聚合。阻碍肌动蛋白丝相互作用的细胞松弛素B抑制了AII刺激的吞噬作用。几乎没有已知激动剂活性的AII类似物阻断了AII刺激的肌动蛋白聚合以及RBC和用IgG调理的RBC的吞噬作用。这些数据支持以下观点:AII与巨噬细胞上的AII受体结合,并可能通过细胞内肌动蛋白的聚合刺激吞噬作用。

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