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Infection and Immunity, October 2006, p. 5465-5476, Vol. 74, No. 10
0019-9567/06/$08.00+0 doi:10.1128/IAI.00737-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Department of Microbiology and Infectious Diseases, Faculty of Medicine, University of Calgary Health Sciences Centre, 3330 Hospital Drive, NW, Calgary, Alberta, Canada T2N 4N1,1 Biosciences Division, Los Alamos National Laboratory, Los Alamos, New Mexico 875452
Received 8 May 2006/ Returned for modification 20 June 2006/ Accepted 28 July 2006
Burkholderia pseudomallei is the causative agent of melioidosis and represents a potential bioterrorism threat. In the current studies we have examined gene expression in B. pseudomallei in an animal model of acute melioidosis using whole-genome microarrays. Gene expression profiles were generated by comparing transcriptional levels of B. pseudomallei-expressed genes in infected hamster organs including liver, lung, and spleen following intraperitoneal and intranasal routes of infection to those from bacteria grown in vitro. Differentially expressed genes were similar in infected livers irrespective of the route of infection. Reduced expression of a number of housekeeping genes suggested a lower bacterial growth rate during infection. Energy production during growth in vivo involved specific biochemical pathways such as isomerization of 3-phosphoglycerate, catabolism of D-glucosamine and inositol, and biosynthesis of particular amino acids. In addition, the induction of genes known to be involved in oxidative phosphorylation including ubiquinol oxidase, ferredoxin oxidoreductase, and formate dehydrogenase enzymes suggested the use of alternative pathways for energy production, while the expression of genes coding for ATP-synthase and NADH-dehydrogenase enzymes was reduced. Our studies have identified differentially expressed genes which include potential virulence genes such as those for a putative phospholipase C and a putative two-component regulatory system, and they have also provided a better understanding of bacterial metabolism in response to the host environment during acute melioidosis.
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