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Induction of macrophage procoagulant activity by Bacteroides fragilis.

机译:脆弱拟杆菌(Bacteroides fragilis)诱导巨噬细胞促凝活性。

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Fibrin deposition in the peritoneal cavity during acute peritonitis appears to predispose the host to abscess formation by providing an environment for bacterial proliferation protected from host defenses. The purpose of the present study was to determine whether the potent abscess-inducing anaerobe Bacteroides fragilis could promote fibrin deposition by inducing mononuclear cells to express procoagulant activity (PCA). B. fragilis stimulated PCA in a dose-dependent fashion, achieving a maximum at 10(7) CFU/ml. Heat-killed B. fragilis induced comparable levels of PCA, while a nonspecific phagocytic stimulus, latex beads, was not stimulatory. B. fragilis was capable of inducing PCA even when phagocytosis was blocked by preexposure of cells to latex beads. The results suggested that phagocytosis was neither necessary nor sufficient for the generation of PCA. Cell separation studies showed that PCA was solely produced by macrophages and that lymphocytes did not augment its production. These studies suggest one potential mechanism by which B. fragilis might initiate abscess formation.
机译:急性腹膜炎期间纤维蛋白在腹膜腔内的沉积似乎通过为细菌增殖提供了免受宿主防御的环境,使宿主易于形成脓肿。本研究的目的是确定强力诱导脓肿的厌氧拟杆菌厌氧菌是否可以通过诱导单核细胞表达促凝活性(PCA)来促进纤维蛋白沉积。脆弱的芽孢杆菌以剂量依赖性方式刺激PCA,在10(7)CFU / ml处达到最大值。热杀死的脆弱脆弱芽孢杆菌可诱导相当水平的PCA,而非特异性吞噬刺激物乳胶珠则无刺激性。即使通过将细胞预先暴露于乳胶珠子来阻止吞噬作用,脆弱的芽孢杆菌也能够诱导PCA。结果表明,吞噬作用对于生成PCA既不是必需的也不是足够的。细胞分离研究表明PCA仅由巨噬细胞产生,而淋巴细胞并未增加其产生。这些研究提示脆弱的芽孢杆菌可能引发脓肿形成的一种潜在机制。

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