The age-related resistance of rats to Plasmodium berghei infection is associated with differential cellular and humoral immune responses

Adam, Estelle; Pierrot, Christine; Lafitte, Sophia; Godin, C.; Saoudi, Abdelhadi; Capron, Moníque; Khalife, Jamal

doi:10.1016/s0020-7519(03)00176-0

Cited by 22 publications

(20 citation statements)

References 62 publications

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“…The Puerto Rican strain of S. mansoni used was maintained in Biomphalaria glabrata snails and golden hamsters. P. berghei ANKA was maintained in Fischer rats as described previously, and parasite extracts were prepared as described by Adam et al (1).…”

Section: Methodsmentioning

confidence: 99%

Identification of a Novel Antigen ofSchistosoma mansoniShared withPlasmodium falciparumand Evaluation of Different Cross-Reactive Antibody Subclasses Induced by Human Schistosomiasis and Malaria

et al. 2006

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Plasmodium falciparum and Schistosoma mansoni are often found in human coinfections, and cross-reactive antibodies to different components of the two parasites have been detected. In this work, we identified a cross-reactive S. mansoni gene product, referred to as SmLRR, that seems to belong to the leucine-rich repeat protein family. Comparative analysis of SmLRR revealed 57% similarity with a putative gene product encoded in the P. falciparum genome. Antibodies to SmLRR were found in experimental infections and in both S. mansoni-and P. falciparum-infected individuals. Correlative analysis of human anti-SmLRR responses in Kenya and Uganda suggested that malaria and schistosomiasis drive the immunoglobulin G3 (IgG3) and IgG4 isotypes, respectively, against SmLRR, suggesting that there is differential regulation of cross-reactive isotypes depending on the infection. In addition, the levels of anti-SmLRR IgG4, but not the levels of IgG3, correlated positively with the intensity of S. mansoni infection.

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Section: Methodsmentioning

confidence: 99%

Identification of a Novel Antigen ofSchistosoma mansoniShared withPlasmodium falciparumand Evaluation of Different Cross-Reactive Antibody Subclasses Induced by Human Schistosomiasis and Malaria

et al. 2006

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“…[220,221]), and it could be hypothesized that the basis for life-long, suppressed IFN-␥ responses against malaria is laid in the immature immune systems of infants in highly endemic areas [222]. However, only little is understood about the effect of age on (cellular) immune responses to malaria from rodent models [223][224][225], and although IFN-␥ responses against malaria in human children growing up in endemic areas tend to be weaker than in adults [61, 68, 226 -228], the effect of prior exposure in these studies is again hard to distinguish from that of age per se.…”

Section: Prevent Exposure-mediated Suppression Of Ifn-␥ Responsesmentioning

confidence: 99%

Interferon-γ—central mediator of protective immune responses against the pre-erythrocytic and blood stage of malaria

McCall

Sauerwein

2010

Journal of Leukocyte Biology

137

113

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Immune responses against Plasmodium parasites, the causative organisms of malaria, are traditionally dichotomized into pre-erythrocytic and blood-stage components. Whereas the central role of cellular responses in pre-erythrocytic immunity is well established, protection against blood-stage parasites has generally been ascribed to humoral responses. A number of recent studies, however, have highlighted the existence of cellular immunity against blood-stage parasites, in particular, the prominence of IFN-γ production. Here, we have undertaken to chart the contribution of this prototypical cellular cytokine to immunity against pre-erythrocytic and blood-stage parasites. We summarize the various antiparasitic effector functions that IFN-γ serves to induce, review an array of data about its protective effects, and scrutinize evidence for any deleterious, immunopathological outcome in malaria patients. We discuss the activation and contribution of different cellular sources of IFN-γ production during malaria infection and its regulation in relation to exposure. We conclude that IFN-γ forms a central mediator of protective immune responses against pre-erythrocytic and blood-stage malaria parasites and identify a number of implications for rational malaria vaccine development.

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“…In contrast, in the rat malaria model, 50 years ago it was observed that young rats (4 weeks old) were highly susceptible to Plasmodium berghei strain infection (mortality > 90%) while adult rats (> 7 weeks old) survived the infection (Zuckerman and Yoeli, 1954; Smalley, 1975). We recently confirmed this observation and showed that young rats infected with PbA could be protected exclusively by adoptive transfer of spleen cells from adult resistant rats (Adam et al ., 2003; Pierrot et al ., 2003). Further analysis by gene profiling of spleen cells transferring immunity revealed the overexpression of genes mainly expressed by eosinophils and neutrophils (Pierrot et al ., 2007).…”

Section: Introductionmentioning

confidence: 57%

Gene profiling analysis reveals the contribution of CD24 and P2Y6R to the susceptibility of young rats to Plasmodium berghei infection

Pierrot¹,

Vampouille²,

Vandomme

et al. 2011

Cellular Microbiology

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SummaryOur previous studies have shown that Plasmodium berghei infection induces distinct clinical, parasitological and immunological states in young susceptible rats versus adult resistant rats. This susceptibility was mainly found to be related to inadequate cellular responses. In this study we first identified the altered genes in young susceptible rats. Unexpectedly, transcriptome analysis did not reveal any alteration of effector cytokines or their receptors. At day 13 p.i., six transcripts corresponding to faim3, mesothelin, gas3 (PMP22), gas7, CD24 and P2Y6R were significantly decreased in young infected rats when compared with adult infected rats. Because CD24 and P2Y6R participate in cellular immune responses, we next evaluated their role in the course of infection. Adoptive transfer experiments showed a transient but robust participation of CD24+ cells in the control of parasitaemia. The role of P2Y6R was investigated via its specific ability to be activated by Uridine di-Phosphate (UDP). Young rats treated with UDP partially restored the expression of P2Y6R, controlled parasitaemia and survived thereafter. In conclusion, this study contributes to the discovery of novel biomarkers in young susceptible rats and suggests that the decrease in their expression could be among the reasons for the development of severe pathology in malaria.

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The age-related resistance of rats to Plasmodium berghei infection is associated with differential cellular and humoral immune responses

Cited by 22 publications

References 62 publications

Identification of a Novel Antigen ofSchistosoma mansoniShared withPlasmodium falciparumand Evaluation of Different Cross-Reactive Antibody Subclasses Induced by Human Schistosomiasis and Malaria

Identification of a Novel Antigen ofSchistosoma mansoniShared withPlasmodium falciparumand Evaluation of Different Cross-Reactive Antibody Subclasses Induced by Human Schistosomiasis and Malaria

Interferon-γ—central mediator of protective immune responses against the pre-erythrocytic and blood stage of malaria

Gene profiling analysis reveals the contribution of CD24 and P2Y6R to the susceptibility of young rats to Plasmodium berghei infection

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