Publications
Reciprocal regulation of immune responses to S. haematobium and P. falciparum in double-infected populations in Northern Senegal.
Diallo TO., Remoué F., and Riveau G.
Update in Tropical Immunology, 2005, 221-233 (PMID : ISBN 81-308-0046-2)
Concomitant or associated infections refer to co-infections in which at least two infectious agents coexist in the same host and are specifically indicated as being genetically different. For individuals living in tropical or subtropical areas, such as Africa, concomitant infections are commonplace. Indeed, co-existing parasitic infections prevail in these areas and are supported by the constant movement of populations, anthropogenic changes but also ecological transformations. Among these cases, co-infections of malaria and helminthiasis are major in Africa and their respective influence on immunity could have consequences for both infection/morbidity developments. The main objective of our immuno-epidemiological approaches, performed in Senegal and presented here, was to evaluate the influence of Plasmodium falciparum and Schistosoma haematobium co-infection on the specific immune responses against these two parasites. The effect on the circulating level of inflammatory immune parameters associated with malaria/schistosomiasis morbidity was also assessed in human populations. In both children and adults, co-infection appeared to be in favour for the increase of acquired protective immune responses specific to malaria and schistosomiasis antigens. Concerning the circulating immune factors associated with both parasite pathologies, co-infection regulated the unbalance between the pro and anti-inflammatory cytokines which could act as harmful effects on the development of malaria/schistosomiasis pathology. Concomitant co-infection could thus orientate_ specific immune responses to an anti-infectious protective profile but could also increase the production of immune parameters associated with morbidity. The multi-infectious status observed in individuals from developing countries could have a major influence on the immune-dependent development of pathologies. This status has to be considered for the control, such as vaccine strategies, ofmajor parasitic diseases.
Schistosomes: the road from host-parasite interactions to vaccines in clinical trials
Capron A, Riveau G, Capron M, Trottein F.
Trends in parasitology, 2005, 21(3):143-9 (PMID : 15734662)
Insights over recent years into the interactions between helminths, including schistosomes, and the immune system have generated new concepts in immunology and significant advances in vaccine strategies. Here, we report recent advances that substantially increase our understanding of the nature of the host innate and adaptive responses to schistosomes and on strategies elaborated by the parasite to manipulate such responses. We also describe the long road that has allowed us to move from the identification of an anti-schistosome vaccine candidate, a 28kDa glutathione-S-transferase, to its recent evaluation in human clinical trials.
Schistosomiasis co-infection in humans influences inflammatory markers in uncomplicated Plasmodium falciparum malaria
Diallo TO, Remoue F, Schacht AM, Charrier N, Dompnier JP, Pillet S, Garraud O, N'diaye AA, Capron A, Capron M, Riveau G.
Parasite immunology, 2004, 26(8-9):365-9 (PMID : 15679634)
Malaria and schistosomiasis are the two major parasite diseases present in developing countries. The epidemiological co-infection with schistosomiasis could influence the development of the physiological reaction associated with Plasmodium falciparum infection in human. Most studies have demonstrated the association of circulating levels of interferon-gamma (IFN-gamma), tumour necrosis factor-a (TNF-alpha), interleukin-10 (IL-10), transforming growth factor (TGF-beta) and soluble Tumour Necrosis Factor Receptors (sTNF-RI and sTNF-RII) with the morbidity of malaria. In the present study, we showed that Schistosoma haematobium co-infection influences, in an age-dependent manner, the unbalance between pro- and anti-inflammatory circulating cytokines that play a key role during malaria infection. Indeed, children co-infected by S. haematobium have higher levels of IFN-gamma and sTNF-RII than children infected only by P. falciparum. In contrast, co-infected adults presented a significant increase of IFN-gamma, IL-10, TGF-beta, sTNF-RI and sTNF-RII rates and IL-10/TNF-alpha ratio. Taken together, this study indicates that schistosomiasis co-infection can unbalance the regulation of inflammatory factors in uncomplicated P. falciparum malaria. The possible consequences of the schistosomiasis co-infection for age-dependent malaria morbidity are discussed.
Specific isotype immune response in the diagnosis of human schistosomiasis pathology?
Bonnard P, Remoue F, Schacht AM, Deuffic-Burban S, Dompnier JP, Elguero E, Charrier N, Cassagnou M, Diop M, Ly A, Capron A, Riveau G.
The American Journal of Tropical Medicine and Hygiene, 2004, 71(2):202-5. (PMID : 15306711 )
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.
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