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Invasion of murine respiratory epithelial cells in vivo by Burkholderia cepacia

C-H. CHIU^*,, A. OSTRY and D.P. SPEERT

*Department of Pediatrics, Chang Gung Children's Hospital, Kweishan 333, Taoyuan, Taiwan, Department of Pathology and Laboratory Medicine and Department of Pediatrics, University of British Columbia, 950 West 28th Avenue, Vancouver, British Columbia V5Z 4H4, Canada

Corresponding author: Dr D.P. Speert.

Received 6 Sept. 2000; revised version received 19 Dec. 2000; accepted 21 Dec. 2001.

Abstract

Pulmonary infections caused by Burkholderia cepacia are an important cause of morbidity and mortality in cystic fibrosis (CF) patients. Several features suggestive of invasion and intracellular sequestration of B. cepacia in CF are persistence of infection in the face of antibiotic therapy and a propensity to cause bacteraemic infections in patients with CF. A mouse respiratory challenge model was used to investigate the invasion phenotype of B. cepacia in vivo. After intratracheal inoculation, epidemic B. cepacia strains translocated from lung to liver and spleen; however, all bacteria were cleared from all organs within 7 days. B. cepacia strains, irrespective of cable piliation, were capable of attaching to and then invading murine respiratory tract epithelial cells. Histopathological examination of lungs showed interstitial infiltrates comprised mainly of polymorphonuclear leucocytes and were associated with widened alveolar septa. Electron microscopy demonstrated B. cepacia within epithelial cells and pulmonary macrophages. This study provides support for in-vitro observations that B. cepacia strains from patients with CF adhere to and then invade respiratory epithelial cells. The invasion phenotype in B. cepacia may be an important virulence factor in CF infections.

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