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Clinical and Diagnostic Laboratory Immunology, May 2003, p. 362-366, Vol. 10, No. 3
1071-412X/03/$08.00+0     DOI: 10.1128/CDLI.10.3.362-366.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Relationship between Plasma Interleukin-12 (IL-12) and IL-18 Levels and Severe Malarial Anemia in an Area of Holoendemicity in Western Kenya

Sujittra Chaisavaneeyakorn,1,2 Caroline Othoro,3 Ya Ping Shi,1,3 Juliana Otieno,4 Sansanee C. Chaiyaroj,2 Altaf A. Lal,1 and Venkatachalam Udhayakumar1*

Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Public Health Service, U.S. Department of Health and Human Services, Atlanta, Georgia 30333,1 Department of Microbiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand,2 Vector Biology and Control Research Center, Kenya Medical Research Institute,3 Ministry of Health, New Nyanza Provincial General Hospital, Kisumu, Kenya4

Received 26 September 2002/ Returned for modification 26 November 2002/ Accepted 27 January 2003

In this study, we investigated whether levels of interleukin-12 (IL-12) and IL-18 in plasma are associated with severe malarial anemia outcomes in an area of holoendemicity in western Kenya. We compared plasma IL-12 and IL-18 levels in six groups of children grouped into the categories aparasitemic, asymptomatic, mild malaria, high-density uncomplicated malaria (UC), moderate malarial anemia (MMA), or severe malarial anemia (SMA). IL-12 levels were significantly reduced in children with SMA (P < 0.05) but not in other groups compared to children in the aparasitemic control group. IL-18, a cytokine known to be critical for the induction of gamma interferon along with IL-12, was produced more frequently (70%) in children with UC (P = 0.06) than in children in the aparasitemic control group (32%). However, in the SMA group the IL-18 response rate declined to 30%, which was similar to that in the aparasitemic control group, which showed a 32% response rate. This finding suggests that the IL-18 response may be impaired in children with SMA. In summary, the results from this study support the hypothesis that impairment of IL-12 and/or IL-18 response may contribute to the development of severe malarial anemia in areas of holoendemicity for malaria.

* Corresponding author. Mailing address: Centers for Disease Control and Prevention, 4770 Buford Highway, Mail Stop F-12, Chamblee, GA 30341. Phone: (770) 488-4862. Fax: (770) 488-4454. E-mail: vxu0{at}cdc.gov.

Clinical and Diagnostic Laboratory Immunology, May 2003, p. 362-366, Vol. 10, No. 3
1071-412X/03/$08.00+0     DOI: 10.1128/CDLI.10.3.362-366.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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  • Boutlis, C. S., Lagog, M., Chaisavaneeyakorn, S., Misukonis, M. A., Bockarie, M. J., Mgone, C. S., Wang, Z., Morahan, G., Weinberg, J. B., Udhayakumar, V., Anstey, N. M. (2003). Plasma Interleukin-12 in Malaria-Tolerant Papua New Guineans: Inverse Correlation with Plasmodium falciparum Parasitemia and Peripheral Blood Mononuclear Cell Nitric Oxide Synthase Activity. Infect. Immun. 71: 6354-6357 [Abstract] [Full Text]  


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