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Infection and Immunity, July 2000, p. 3888-3893, Vol. 68, No. 7
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

The CXC Chemokines Gamma Interferon (IFN-gamma )-Inducible Protein 10 and Monokine Induced by IFN-gamma Are Released during Severe Melioidosis

Fanny N. Lauw,1,2 Andrew J. H. Simpson,3,4 Jan M. Prins,2 Sander J. H. van Deventer,1 Wipada Chaowagul,5 Nicholas J. White,3,4 and Tom van der Poll1,2,*

Laboratory of Experimental Internal Medicine1 and Department of Infectious Diseases, Tropical Medicine and AIDS,2 Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand3; Centre for Tropical Medicine, Nuffield Department of Clinical Medicine, John Radcliffe Hospital, University of Oxford, Oxford, United Kingdom4; and Sappasitprasong Hospital, Ubon Ratchathani, Thailand5

Received 10 January 2000/Returned for modification 1 March 2000/Accepted 14 April 2000

Gamma interferon (IFN-gamma )-inducible protein 10 (IP-10) and monokine induced by IFN-gamma (Mig) are related CXC chemokines which bind to the CXCR3 receptor and specifically target activated T lymphocytes and natural killer (NK) cells. The production of IP-10 and Mig by various cell types in vitro is strongly dependent on IFN-gamma . To determine whether IP-10 and Mig are released during bacterial infection in humans, we measured plasma levels of IP-10 and Mig in patients with melioidosis, a severe gram-negative infection caused by Burkholderia pseudomallei. IP-10 and Mig were markedly elevated in patients with melioidosis on admission, particularly in blood culture-positive patients, and remained elevated during the 72-h study period. Levels of IP-10 and Mig showed a positive correlation with IFN-gamma concentrations and also correlated with clinical outcome. In whole blood stimulated with heat-killed B. pseudomallei, neutralization of IFN-gamma and tumor necrosis factor alpha (TNF-alpha ) partly attenuated IP-10 and Mig release, while anti-interleukin-12 (IL-12) and anti-IL-18 had a synergistic effect. Stimulation with other bacteria or endotoxin also induced strong secretion of IP-10 and Mig. These data suggest that IP-10 and Mig are part of the innate immune response to bacterial infection. IP-10 and Mig may contribute to host defense in Th1-mediated host defense during infections by attracting CXCR3+ Th1 cells to the site of inflammation.

* Corresponding author. Mailing address: Laboratory of Experimental Internal Medicine, Rm. G2-132, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. Phone: 31-20-5669111. Fax: 31-20-6977192. E-mail: T.vanderpoll{at}amc.uva.nl.

Infection and Immunity, July 2000, p. 3888-3893, Vol. 68, No. 7
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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