Hepatosplenomegaly is associated with low regulatory and Th2 responses to schistosome antigens in childhood schistosomiasis and malaria coinfection

Shona Wilson, Francis M. Jones, Joseph K. Mwatha, Gachuhi Kimani, Mark Booth, H. Curtis Kariuki, Birgitte J Vennervald, John H. Ouma, Eric Muchiri, David W. Dunne

    30 Citations (Scopus)

    Abstract

    Hepatosplenomegaly among 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 may be due to
    immunological inflammation. For a cohort of school-age 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 the levels were negatively
    correlated with S. mansoni infection intensities and were lower among children
    who were coinfected with P. falciparum. Tumor necrosis factor alpha levels in
    response to stimulation with SEA were high, and a negative association between
    presentation with hepatomegaly and the levels of the regulatory cytokines
    interleukin-6 and transforming growth factor beta(1) suggests that a possible
    mechanism for childhood hepatomegaly in areas where both malaria and
    schistosomiasis are endemic is poor regulation of an inflammatory response to
    schistosome eggs.
    Original languageEnglish
    JournalInfection and Immunity
    Volume76
    Issue number5
    Pages (from-to)2212-2218
    Number of pages7
    ISSN0019-9567
    DOIs
    Publication statusPublished - 2008

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