Schistosomiasis coinfection in children influences acquired immune response against Plasmodium falciparum malaria antigens.

BACKGROUND: Malaria and schistosomiasis coinfection frequently occurs in tropical countries. This study evaluates the influence of Schistosoma haematobium infection on specific antibody responses and cytokine production to recombinant merozoite surface protein-1-19 (MSP1-(19)) and schizont extract of Plasmodium falciparum in malaria-infected children. METHODOLOGY: Specific IgG1 to MSP1-(19), as well as IgG1 and IgG3 to schizont extract were significantly increased in coinfected children compared to P. falciparum mono-infected children. Stimulation with MSP1-(19) lead to a specific production of both interleukin-10 (IL-10) and interferon-γ (IFN-γ), whereas the stimulation with schizont extract produced an IL-10 response only in the coinfected group. CONCLUSIONS: Our study suggests that schistosomiasis coinfection favours anti-malarial protective antibody responses, which could be associated with the regulation of IL-10 and IFN-γ production and seems to be antigen-dependent. This study demonstrates the importance of infectious status of the population in the evaluation of acquired immunity against malaria and highlights the consequences of a multiple infection environment during clinical trials of anti-malaria vaccine candidates.

Specific isotype immune response in the diagnosis of human schistosomiasis pathology?

Since the few indirect markers available for assessing the development and the stage of intestinal schistosomiasis morbidity are weakly specific, endoscopy is still the only method able to detect severe forms of pathology. Therefore, we evaluated the isotype antibody response to the current schistosome antigen preparation (soluble egg antigens [SEA]) in 142 Senegalese patients infected with Schistosoma mansoni. They were stratified into three different stages of pathology according to ultrasonographic, endoscopic, and clinical parameters (stage 1 = no detectable pathology; stage 2 = moderate morbidity; stage 3 = severe forms of pathology). Only median specific IgG4, IgE, and IgA responses changed according to the stage of pathology. The IgA level was significantly higher in stages 2 and 3 compared with stage 1, and the IgE level was higher in stage 3 compared with stage 1. A high specific IgG4 level was observed only in stage 3 and was significantly different compared with stage 2. We show an association between the variability of the specific response to SEA and the degree of morbidity, and demonstrate that IgA and IgG4 responses could be combined markers to easily discriminate the different stages of pathology due to infection with S. mansoni.