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Infect Immun. 1989 March; 57(3): 817-822

Stimulation by fibronectin of macrophage-mediated phagocytosis of Pseudomonas aeruginosa.

J L Kluftinger, N M Kelly and R E Hancock

Department of Microbiology, University of British Columbia, Vancouver, Canada.

ABSTRACT

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.


Infect Immun. 1989 March; 57(3): 817-822







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