Rosenthal G A, Levy G, Rotstein O D
Department of Surgery, Toronto General Hospital, Ontario, Canada.
Infect Immun. 1989 Feb;57(2):338-43. doi: 10.1128/iai.57.2.338-343.1989.
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.
急性腹膜炎时腹腔内纤维蛋白沉积,似乎通过为细菌增殖提供一个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具有强大脓肿诱导能力的厌氧菌脆弱拟杆菌是否可通过诱导单核细胞表达促凝活性(PCA)来促进纤维蛋白沉积。脆弱拟杆菌以剂量依赖方式刺激PCA,在10⁷CFU/ml时达到最大值。热灭活的脆弱拟杆菌诱导出相当水平的PCA,而一种非特异性吞噬刺激物乳胶珠则无刺激作用。即使细胞预先接触乳胶珠使吞噬作用受阻,脆弱拟杆菌仍能够诱导PCA。结果表明,吞噬作用对于PCA的产生既非必要条件也非充分条件。细胞分离研究显示,PCA仅由巨噬细胞产生,淋巴细胞不会增加其产生。这些研究提示了脆弱拟杆菌可能引发脓肿形成的一种潜在机制。