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Infection and Immunity, October 2009, p. 4337-4344, Vol. 77, No. 10
0019-9567/09/$08.00+0     doi:10.1128/IAI.00259-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Virulence and Cellular Interactions of Burkholderia multivorans in Chronic Granulomatous Disease{triangledown}

Adrian M. Zelazny,1,4* Li Ding,1 Houda Z. Elloumi,1,{dagger} Lauren R. Brinster,2 Fran Benedetti,2 Meggan Czapiga,3,{ddagger} Ricky L. Ulrich,5,§ Samuel J. Ballentine,1 Joanna B. Goldberg,6 Elizabeth P. Sampaio,1,7 and Steven M. Holland1

Laboratory of Clinical Infectious Diseases,1 Division of Veterinary Resources,2 Biological Imaging Section, NIAID,3 Microbiology Service, Clinical Center, National Institutes of Health, Bethesda, Maryland,4 Bacteriology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland,5 Department of Microbiology, University of Virginia Health System, Charlottesville, Virginia,6 Leprosy Laboratory, Oswaldo Cruz Institute, FIOCRUZ, Rio de Janeiro, Brazil7

Received 5 March 2009/ Returned for modification 1 June 2009/ Accepted 22 July 2009

Chronic granulomatous disease (CGD) patients are susceptible to life-threatening infections by the Burkholderia cepacia complex. We used leukocytes from CGD and healthy donors and compared cell association, invasion, and cytokine induction by Burkholderia multivorans strains. A CGD isolate, CGD1, showed higher cell association than that of an environmental isolate, Env1, which correlated with cell entry. All B. multivorans strains associated significantly more with cells from CGD patients than with those from healthy donors. Similar findings were observed with another CGD pathogen, Serratia marcescens, but not with Escherichia coli. In a mouse model of CGD, strain CGD1 was virulent while Env1 was avirulent. B. multivorans organisms were found in the spleens of CGD1-infected mice at levels that were 1,000 times higher than those found in Env1-infected mice, which was coincident with higher levels of the proinflammatory cytokine interleukin-1β. Taken together, these results may shed light on the unique susceptibility of CGD patients to specific pathogens.

* Corresponding author. Mailing address: Microbiology Service, Department of Laboratory Medicine, National Institutes of Health, 10 Center Dr., Bldg. 10/2C-385, Bethesda, MD 20892. Phone: (301) 496-6200. Fax: (301) 402-1886. E-mail: azelazny{at}mail.nih.gov

{triangledown} Published ahead of print on 27 July 2009.

Editor: V. J. DiRita

{dagger} Present address: Department of Medicine, Division of Gastroenterology and Hepatology, University of North Carolina, Chapel Hill, NC.

{ddagger} Present address: Medimmune Inc., Gaithersburg, MD.

§ Present address: Math and Science, Hagerstown Community College, Hagerstown, MD.

Infection and Immunity, October 2009, p. 4337-4344, Vol. 77, No. 10
0019-9567/09/$08.00+0     doi:10.1128/IAI.00259-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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