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Infection and Immunity, June 2007, p. 3074-3079, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01733-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

High-Throughput mRNA Profiling Characterizes the Expression of Inflammatory Molecules in Sepsis Caused by Burkholderia pseudomallei

W. Joost Wiersinga,^1,2* Mark C. Dessing,^1,2 Piet A. Kager,¹ Allen C. Cheng,³ Direk Limmathurotsakul,⁴ Nicholas P. Day,^4,5 Arjen M. Dondorp,⁴ Tom van der Poll,^1,2 and Sharon J. Peacock^4,5

Center for Infection and Immunity Amsterdam,¹ Center for Experimental and Molecular Medicine, Academic Medical Center, 1105 AZ Amsterdam, The Netherlands,² Menzies School of Health Research, Charles Darwin University, Darwin, Australia,³ Wellcome Trust, Faculty of Tropical Medicine, Mahidol University, 10400 Bangkok, Thailand,⁴ Centre for Clinical Vaccinology and Tropical Medicine, University of Oxford, Oxford, England⁵

Received 31 October 2006/ Returned for modification 17 December 2006/ Accepted 11 March 2007

Sepsis is characterized by an uncontrolled inflammatory response to invading microorganisms. We describe the inflammatory mRNA profiles in whole-blood leukocytes, monocytes, and granulocytes using a multigene system for 35 inflammatory markers that included pro- and anti-inflammatory cytokines, chemokines, and signal transduction molecules in a case-control study with 34 patients with sepsis caused by the gram-negative bacterium Burkholderia pseudomallei (the pathogen causing melioidosis) and 32 healthy volunteers. Relative to healthy controls, patients with sepsis showed increased transcription of a whole array of inflammatory genes in peripheral blood leukocytes, granulocytes, and monocytes. Specific monocyte and granulocyte mRNA profiles were identified. Strong correlations were found between inflammatory mRNA expression levels in monocytes and clinical outcome. These data underline the notion that circulating leukocytes are an important source for inflammatory mediators in patients with gram-negative sepsis. Gene profiling such as was done here provides an excellent tool to obtain insight into the extent of inflammation activation in patients with severe infection.

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* Corresponding author. Mailing address: Academic Medical Center, Meibergdreef 9, Room G2-132, 1105 AZ Amsterdam, The Netherlands. Phone: 31-20-5669111. Fax: 31-20-6977192. E-mail: w.j.wiersinga{at}amc.uva.nl

Published ahead of print on 19 March 2007.

Editor: A. Camilli

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Infection and Immunity, June 2007, p. 3074-3079, Vol. 75, No. 6
0019-9567/07/$08.00+0     doi:10.1128/IAI.01733-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

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