Coinfections withSchistosoma haematobium, Necator americanusandEntamoeba histolytica/Entamoeba disparin Children: Chemokine and Cytokine Responses and Changes after Antiparasite Treatment

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Abstract

The effect of polyparasite infections on cytokine and chemokine responses as well as the effect of antiparasite treatment was studied in children without parasite infection (the G0 group), in children singly infected withSchistosoma haematobium(the G1 group), and in children multiply infected withS. haematobium/Schistosoma mansoni, Entamoeba histolytica/Entamoeba disparandNecator americanus(the G3+ group). Linear regression analysis disclosed a significant risk for coinfection with hookworm andSchistosomaspecies. Polyparasite infections detected in 23% of children before treatment were present in 5% at 15 months after treatment. Chemokine responses toS. mansoniadult worm antigen (SmAg) diminished after treatment for macrophage inflammatory chemokine (MIP)-1α/chemokine (C-C motif) ligand (CCL)-3 (among G3+ children, by a factor of 200 [95% confidence interval {CI}, 33-1111]) and for MIP-1β/CCL-4 (among G3+ children, by a factor of 26 [95% CI, 6-117]) but were enhanced for thymus- and activation-regulated chemokine/CCL-17 (among G3+ children, by a factor of 10 [95% CI, 3-32]) (P<.001 for all). In response toE. histolyticaantigen, interleukin (IL)-13 levels increased after treatment among G1 children by a factor of 138 (95% CI, 12-1569) and among G3+ children by a factor of 21 (95% CI, 7-64) (P<.001 for both). Cellular production of interferon (IFN)-γ in response to SmAg decreased 4 weeks after treatment among G3+ children, whereas T helper cell type 2 (Th2) IL-13 production was enhanced among G1 and G3+ children. In summary, polyparasite infections withS. haematobium/S. mansoni, E. histolytica/E. disparandN. americanusgenerated prominent proinflammatory cytokine and chemokine responses, and, after antihelminth treatment, the inflammatory chemokine response lessened as the Th2 responsiveness in coinfected children increased.

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