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Infection and Immunity, January 2000, p. 24-29, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Invasion and Intracellular Survival of Burkholderia cepacia

Daniel W. Martin1 and Christian D. Mohr2,*

Department of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, North Carolina 27834,1 and Department of Microbiology, University of Minnesota, Minneapolis, Minnesota 554552

Received 22 July 1999/Returned for modification 20 September 1999/Accepted 1 October 1999

Burkholderia cepacia has emerged as an important pulmonary pathogen in immunocompromised patients and in patients with cystic fibrosis (CF). Little is known about the virulence factors and pathogenesis of B. cepacia, although the persistent and sometimes invasive infections caused by B. cepacia suggest that the organism possesses mechanisms for both cellular invasion and evasion of the host immune response. In this study, cultured human cells were used to analyze the invasion and intracellular survival of B. cepacia J2315, a highly transmissible clinical isolate responsible for morbidity and mortality in CF patients. Quantitative invasion and intracellular growth assays demonstrated that B. cepacia J2315 was able to enter, survive, and replicate intracellularly in U937-derived macrophages and A549 pulmonary epithelial cells. Transmission electron microscopy of infected macrophages confirmed the presence of intracellular B. cepacia and showed that intracellular bacteria were contained within membrane-bound vacuoles. An environmental isolate of B. cepacia, strain J2540, was also examined for its ability to invade and survive intracellularly in cultured human cells. J2540 entered cultured macrophages with an invasion frequency similar to that of the clinical strain, but it was less invasive than the clinical strain in epithelial cells. In marked contrast to the clinical strain, the environmental isolate was unable to survive or replicate intracellularly in either cultured macrophages or epithelial cells. Invasion and intracellular survival may play important roles in the ability of virulent strains of B. cepacia to evade the host immune response and cause persistent infections in CF patients.

* Corresponding author. Mailing address: Department of Microbiology, University of Minnesota, 1460 Mayo Memorial Bldg., Box 196, 420 Delaware St. SE, Minneapolis MN 55455-0312. Phone: (612) 625-7104. Fax: (612) 626-0623. E-mail: mohr{at}lenti.med.umn.edu.

Infection and Immunity, January 2000, p. 24-29, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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