Infect. Immun. doi:10.1128/IAI.01433-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
Childhood schistosomiasis and malaria co-infection: hepatosplenomegaly is associated with low regulatory and Th2 responses to schistosome antigens
Shona Wilson*,
Frances M. Jones,
Joseph K. Mwatha,
Gachuhi Kimani,
Mark Booth,
H. Curtis Kariuki,
Birgitte J. Vennervald,
John H. Ouma,
Eric Muchiri,
and
David W. Dunne
Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, United Kingdom; Kenya Medical Research Institute, Nairobi, Kenya; Division of Vector Borne Diseases, Kenyan Ministry of Health, PO Box 54840 Nairobi, Kenya; DBL – Institute for Health Research and Development, Jægersborg Alle 1D, 2920 Charlottenlund, Denmark; Maseno University, Kisumu, Kenya
* To whom correspondence should be addressed. Email:
sw320{at}cam.ac.uk.
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Abstract |
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Hepatosplenomegaly amongst Kenyan schoolchildren has been shown to be exacerbated where there is transmission of both Schistosoma mansoni and Plasmodium falciparum. This highly prevalent and chronic morbidity often occurs in the absence of ultrasound detectable periportal fibrosis and maybe due to immunological inflammation. For a cohort of school-aged children, whole blood cultures were stimulated with S. mansoni soluble egg antigen (SEA) or soluble worm antigen (SWA). Responses to SWA were found to be predominantly Th2 cytokines, however, they were not significantly associated with either hepatosplenomegaly or infection with S. mansoni or P. falciparum. In comparison, SEA specific Th2 cytokine responses were low and levels were negatively correlated with S. mansoni infection intensities and were lower amongst children who were co-infected with P. falciparum. TNF
levels in response to stimulation with SEA were high, and a negative association between presentation with hepatomegaly and levels of the regulatory cytokines IL-6 and TGF
1, suggests that a possible mechanism for childhood hepatomegaly in malaria/schistosomiasis co-endemic areas is poor regulation of an inflammatory response to schistosome eggs.