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IL-33, a proposed alarmin, stimulates innate immune cells and Th2 cells to produce IL-13 and is rapidly upregulated upon antigen exposure in murine helminth infection. The human IL-33 response to helminth antigen was analysed in Malians infected with Schistosoma haematobium by disrupting parasite integrity via chemotherapy. Plasma IL-33 was measured pretreatment, and 24 h and 9 weeks post-treatment. At 24 h post-treatment, IL-33 levels were low. Nine week post-treatment IL-33 levels were elevated and were associated with an increase in intracellular IL-13 in eosinophils. Up-regulation of intracellular IL-13 in eosinophils was also associated with eosinophil expression of ST2L, the IL-33 receptor. IL-33 may play an important downstream role in the human response to schistosome adult worm antigen exposure. [ABSTRACT FROM AUTHOR]

In sub-Saharan Africa, chronic hepatosplenomegaly, with palpable firm/hard organ consistency, is common, particularly among school-aged children. This morbidity can be caused by long-term exposure to malaria, or by Schistosoma mansoni , and it is exacerbated when these two occur together. Although immunological mechanisms probably underlie the pathogenic process, these mechanisms have not been identified, nor is it known whether the two parasites augment the same mechanisms or induce unrelated processes that nonetheless have additive or synergistic effects. Kenyan primary schoolchildren, living in a malaria/schistosomiasis co-transmission area, participated in cross-sectional parasitological and clinical studies in which circulating immune modulator levels were also measured. Plasma IL-12p70, sTNF-RII, IL-10 and IL-13 levels correlated with relative exposure to malaria, and with hepatosplenomegaly. Soluble-TNF-RII and IL-10 were higher in children infected with S. mansoni . Hepatosplenomegaly caused by chronic exposure to malaria was clearly associated with increased circulating levels of pro-inflammatory mediators, with higher levels of regulatory modulators, and with tissue repair cytokines, perhaps being required to control the inflammatory response. The higher levels of regulatory modulators amongst S. mansoni infected children, compared to those without detectable S. mansoni and malarial infections, but exposed to malaria, suggest that S. mansoni infection may augment the underlying inflammatory reaction. [ABSTRACT FROM AUTHOR]

The changes in the immune responses of patients before and at 3 weeks after treatment with antischistosomal drugs were investigated. Lymphocyte responses to Concanavalin A and to worm antigens were inhibited after treatment, whereas responses to cercarial and egg antigens remained unchanged. Eosinophil levels were significantly elevated after treatment and were positively correlated with the increase in anti-worm antibodies (r = 0.587), and negatively associated with anti-egg antibodies (r= -0.727). Although the eosinophil-dependent cytotoxicity to schistosomula was not significantly enhanced after treatment, some increased killing was evident in half the patients (7,15). On the other hand, the ability of adherent mononuclear cells to stimulate eosinophil functions was markedly enhanced by treatment (P < 0.001). These studies suggest that treatment may enhance some of the potentially protective host's immune mechanisms. [ABSTRACT FROM AUTHOR]