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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/25979
Title: The CXC chemokines gamma interferon (IFN-γ)-inducible protein 10 and monokine induced by IFN-γ are released during severe melioidosis
Authors: Fanny N. Lauw
Andrew J.H. Simpson
Jan M. Prins
Sander J.H. Van Deventer
Wipada Chaowagul
Nicholas J. White
Tom Van Der Poll
Academic Medical Centre, University of Amsterdam
Mahidol University
University of Oxford
Sappasitthiprasong Hospital
Keywords: Immunology and Microbiology;Medicine
Issue Date: 1-Jul-2000
Citation: Infection and Immunity. Vol.68, No.7 (2000), 3888-3893
Abstract: Gamma interferon (IFN-γ)-inducible protein 10 (IP-10) and monokine induced by IFN-γ (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-γ. 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-γ concentrations and also correlated with clinical outcome. In whole blood stimulated with heat-killed B. pseudomallei, neutralization of IFN-γ and tumor necrosis factor alpha (TNF-α) 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.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=0033917847&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/25979
ISSN: 00199567
Appears in Collections:Scopus 1991-2000

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