Kluftinger J L, Kelly N M, Hancock R E
Department of Microbiology, University of British Columbia, Vancouver, Canada.
Infect Immun. 1989 Mar;57(3):817-22. doi: 10.1128/iai.57.3.817-822.1989.
In a previous investigation it was determined that Pseudomonas aeruginosa cells taken directly from a mouse in vivo growth system were significantly more susceptible to nonopsonic phagocytosis by macrophages than were similar cells after being washed in buffer (N. M. Kelly, J. L. Battershill, S. Kuo, J. P. Arbuthnott, and R. E. W. Hancock, Infect. Immun. 55:2841-2843, 1987). It was demonstrated that a phagocytosis-promoting factor was found in the supernatant obtained from chambers incubated in the peritoneal cavities of laboratory mice or rats. The phagocytosis-promoting factor was effective with both strains of P. aeruginosa tested, using both unelicited mouse peritoneal macrophages and the P388D1 mouse macrophage cell line as the phagocytic cells. Phagocytosis enhancement was observed with in vivo-grown bacteria and with bacteria grown in vitro on agar plates, but not with bacteria grown in vitro with rapid agitation. Supernatants from mice and rats were fractionated using a fast pressure liquid chromatography gel exclusion column. The phagocytosis-promoting factor copurified with fibronectin. Furthermore, antifibronectin sera negated the phagocytosis-promoting activities of in vivo chamber supernatant, while commercial bovine fibronectin was itself capable of promoting phagocytosis. The concentrations of fibronectin increased in both rat and mouse peritoneal chambers with time, coincident with the ability of chamber supernatants to promote phagocytosis. It was concluded that fibronectin was the phagocytosis-promoting factor of chamber supernatants. Bacterial presence in the peritoneal chambers was not required to elicit fibronectin uptake into the chambers.
在先前的一项研究中发现,直接取自小鼠体内生长系统的铜绿假单胞菌细胞,比在缓冲液中洗涤后的类似细胞更容易被巨噬细胞进行非调理吞噬作用(N.M.凯利、J.L.巴特希尔、S.郭、J.P.阿巴思诺特和R.E.W.汉考克,《感染与免疫》55:2841 - 2843,1987年)。结果表明,在实验室小鼠或大鼠腹腔内培养腔室获得的上清液中发现了一种促进吞噬作用的因子。使用未刺激的小鼠腹腔巨噬细胞和P388D1小鼠巨噬细胞系作为吞噬细胞,该促进吞噬作用的因子对所测试的两种铜绿假单胞菌菌株均有效。观察到体内生长的细菌以及在琼脂平板上体外生长的细菌的吞噬作用增强,但在快速搅拌下体外生长的细菌则没有这种现象。使用快速压力液相色谱凝胶排阻柱对小鼠和大鼠的上清液进行分级分离。促进吞噬作用的因子与纤连蛋白共纯化。此外,抗纤连蛋白血清消除了体内培养腔室上清液的促进吞噬作用活性,而商业牛纤连蛋白本身能够促进吞噬作用。随着时间的推移,大鼠和小鼠腹腔内培养腔室中纤连蛋白的浓度均升高,这与培养腔室上清液促进吞噬作用的能力相一致。得出的结论是,纤连蛋白是培养腔室上清液中促进吞噬作用的因子。腹腔内培养腔室中不需要有细菌存在来引发纤连蛋白进入腔室。