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Infection and Immunity, February 2004, p. 728-734, Vol. 72, No. 2
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.2.728-734.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Cytokine Production in Whole Blood Cultures from a Fishing Community in an Area of High Endemicity for Schistosoma mansoni in Uganda: the Differential Effect of Parasite Worm and Egg Antigens
Sarah Joseph,1* Frances M. Jones,1 Gachuhi Kimani,2 Joseph K. Mwatha,2 Timothy Kamau,2 Francis Kazibwe,3 Jovanice Kemijumbi,3 Narcis B. Kabatereine,3 Mark Booth,1 Henry C. Kariuki,4 John H. Ouma,2 Birgitte J. Vennervald,5 and David W. Dunne1
Department of Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom,1
Kenya Medical Research Institute,2
Division of Vector Borne Diseases, Nairobi, Kenya,4
Vector Control Division, Kampala, Uganda,3
Danish Bilharziasis Laboratory, Charlottenlund, Denmark5
Received 7 July 2003/
Returned for modification 3 September 2003/
Accepted 14 October 2003
The human host is continuously exposed to the egg and the adult worm developmental stages of Schistosoma mansoni during chronic infections with the parasite. To assess the cytokine responses induced by these different costimulating stages and how they are influenced by host age and infection intensity, whole blood samples from a cross-sectional cohort of 226 members of a Ugandan fishing community who had been resident in an area with high transmission of S. mansoni for the previous 10 years or from birth were stimulated with S. mansoni egg antigen (SEA) or worm antigen (SWA). SWA-specific gamma interferon (IFN-
) production increased with age, and the levels of SWA- and SEA-specific interleukin 3 (IL-3) were weakly correlated with schistosome infection intensity. The production of most cytokines was little affected by age or infection intensity but was either SEA or SWA specific. One hundred thirty-two members of the cohort coproduced IL-5 and IL-13 specifically in response to SWA, whereas only 15 produced these cytokines, and at much lower levels, in response to SEA. IL-10, IL-4, and IFN-
were also produced in response to SWA, whereas the response to SEA consisted almost exclusively of IL-10. Our results suggest that, in contrast to what has been described for the murine model of S. mansoni and during acute human infections, chronic intense exposure to and infection with S. mansoni in this cohort resulted in very low levels of response to SEA in vitro in the presence of a vigorous and mixed Th1-Th2 response to SWA.
* Corresponding author. Mailing address: University of Cambridge, Dept. of Pathology, Tennis Court Rd., Cambridge CB2 1QP, United Kingdom. Phone: 44-1223333332. Fax: 44-1223333741. E-mail: sj122{at}cam.ac.uk.
Jovanice Kemijumbi passed away during the preparation of this paper. She made a major contribution to the work presented here and is greatly missed.
Editor: W. A. Petri, Jr.
Infection and Immunity, February 2004, p. 728-734, Vol. 72, No. 2
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.2.728-734.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
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Copyright © 2004 by the American Society for Microbiology. All rights reserved.