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Infection and Immunity, December 2008, p. 5447-5455, Vol. 76, No. 12
0019-9567/08/$08.00+0     doi:10.1128/IAI.00451-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

A Type IV Secretion System Contributes to Intracellular Survival and Replication of Burkholderia cenocepacia{triangledown}

S. Umadevi Sajjan,1 Lisa A. Carmody,1 Carlos F. Gonzalez,2 and John J. LiPuma1*

Department of Pediatrics and Communicable Disease, University of Michigan Medical School, Ann Arbor, Michigan 48109,1 Department of Plant Pathology and Microbiology, Texas A&M University, College Station, Texas 778432

Received 11 April 2008/ Returned for modification 13 May 2008/ Accepted 16 September 2008

Burkholderia cenocepacia is an important respiratory pathogen in persons with cystic fibrosis (CF). Recent studies indicate that B. cenocepacia survives within macrophages and airway epithelial cells in vitro by evading endosome-lysosome fusion. We investigated the role of a plasmid-encoded type IV secretion system in the intracellular survival, replication, and processing of B. cenocepacia. Both a wild-type strain (K56-2) and its type IV secretion system mutant (designated LC101) entered and replicated in CF airway epithelial cells and monocyte-derived macrophages. However, significantly more intracellular K56-2 than LC101 bacteria were found in both cell types at 24 h postinfection. Colocalization of bacteria with markers of the classical endocytic pathway indicated that although both K56-2 and LC101 reside transiently in early endosomes, a greater proportion of the mutant bacteria are targeted to lysosomal degradation. In contrast, wild-type bacteria escape from the classical endocytic pathway and traffic to the endoplasmic reticulum, where they replicate. Our results show that the intracellular processing of B. cenocepacia is similar in both professional and nonprofessional phagocytes and that a functional plasmid-encoded type IV secretion system contributes to the survival and replication of B. cenocepacia in eukaryotic cells.

* Corresponding author. Mailing address: Department of Pediatrics and Communicable Diseases, University of Michigan Medical School, 1150 W. Medical Center Drive, 8323 MSRB III, SPC 5646, Ann Arbor, MI 48109. Phone: (734) 936-9767. Fax: (734) 764-4279. E-mail: jlipuma{at}umich.edu

{triangledown} Published ahead of print on 29 September 2008.

Editor: J. B. Bliska

Infection and Immunity, December 2008, p. 5447-5455, Vol. 76, No. 12
0019-9567/08/$08.00+0     doi:10.1128/IAI.00451-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Keith, K. E., Hynes, D. W., Sholdice, J. E., Valvano, M. A. (2009). Delayed association of the NADPH oxidase complex with macrophage vacuoles containing the opportunistic pathogen Burkholderia cenocepacia. Microbiology 155: 1004-1015 [Abstract] [Full Text]  


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