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Microarray based analysis of temperature and oxidative stress induced messenger RNA in Schistosoma mansoni

ABSTRACT: The body’s defense against schistosome infection can take many forms. For example, upon developing acute schistosomiasis, patients often have fever coinciding with larval maturation, migration and early oviposition. As the infection becomes established, the parasite comes under oxidative stress generated by the host immune system. The most common treatment for schistosomiasis is the anti-helmenthic drug praziquantel. Its effectiveness, however, is limited due to its inability to kill schistosomes 2 - 4 weeks post-infection. Clearly there is a need for new anti-schistosomal drugs. We hypothesize that gene products expressed as part of a protective response against heat and/or oxidative stress are potential therapeutic targets for future drug development. Using a 12,166 element oligonucleotide microarray to characterize Schistosoma mansoni genes induced by heat and oxidative stress we found that 1,878 Schistosoma mansoni elements were significantly induced by heat stress. These included previously reported heat-shock genes expressing homologs of HSP40, HSP70 and HSP86. One thousand and one elements were induced by oxidative stress including those expressing homologs of superoxide dismutase, glutathione peroxidase and aldehyde dehydrogenase. Seventy-two elements were common to both stressors that could potentially be exploited in the development of novel anti-schistosomal therapeutics. Keywords: Stress response, time course

ORGANISM(S): Schistosoma mansoni

PROVIDER: GSE11706 | GEO | 2008/08/25

SECONDARY ACCESSION(S): PRJNA106121

REPOSITORIES: GEO

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Microarray based analysis of temperature and oxidative stress induced messenger RNA in Schistosoma mansoni

Project description:The body’s defense against schistosome infection can take many forms. For example, upon developing acute schistosomiasis, patients often have fever coinciding with larval maturation, migration and early oviposition. As the infection becomes established, the parasite comes under oxidative stress generated by the host immune system. The most common treatment for schistosomiasis is the anti-helmenthic drug praziquantel. Its effectiveness, however, is limited due to its inability to kill schistosomes 2 - 4 weeks post-infection. Clearly there is a need for new anti-schistosomal drugs. We hypothesize that gene products expressed as part of a protective response against heat and/or oxidative stress are potential therapeutic targets for future drug development. Using a 12,166 element oligonucleotide microarray to characterize Schistosoma mansoni genes induced by heat and oxidative stress we found that 1,878 Schistosoma mansoni elements were significantly induced by heat stress. These included previously reported heat-shock genes expressing homologs of HSP40, HSP70 and HSP86. One thousand and one elements were induced by oxidative stress including those expressing homologs of superoxide dismutase, glutathione peroxidase and aldehyde dehydrogenase. Seventy-two elements were common to both stressors that could potentially be exploited in the development of novel anti-schistosomal therapeutics. Keywords: Stress response, time course Eight samples performed in duplicate for each temperature and oxidative stresses at time points 0, 30, 60, and 240 min over a common reference sample for each stress

2008-08-25 | E-GEOD-11706 | biostudies-arrayexpress

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Effect of Praziquantel on the Differential Expression of Mouse Hepatic Genes and Parasite ATP Binding Cassette Transporter Gene Family Members During Schistosoma mansoni Infection

Project description:Schistosomiasis is a disease caused by parasitic worms that significantly impacts on the lives of approximately 250 million people. During infection, female parasites release thousands of eggs, a significant number of which become trapped in the liver. The entrapment of the eggs triggers immune and inflammatory responses that in turn cause many of the health problems associated with the disease. In this study we analyzed the gene expression profiles of livers from mice infected with the human parasite Schistosoma mansoni over multiple time points, beginning when the parasites start to lay eggs. Mice were treated with a lethal dose of the anti-schistosomal drug praziquantel, and we identified a number of different genes and pathways that are central to immune and inflammatory responses that are active even in the absence of egg deposition. Praziquantel is the only drug available to treat schistosomiasis, however it is ineffective against juvenile parasites during the early stages of mammalian infection. We also show that the development of drug resistance may be due to the improved efficacy of the juvenile parasite to actively excrete the drug. These results provide insights into the effect of praziquantel on the host response to infection as well as ability of juvenile parasites to overcome the lethal effect of the drug.

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Project description:Schistosoma mansoni is the causative agent of schistosomiasis, an endemic neglected tropical disease that affects the human population. Recently, newer versions of the genome and transcriptome have been published, with the Sanger Institute leading both the original publication of the genome as well as the further upgrade. However, little is known about the regulatory elements found in the genome, i.e. promoters. Identification of these elements is key for the understanding of mechanisms of regulation of gene expression in this parasitic helminth.

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2019-09-26 | PXD015129 | Pride

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Project description:Schistosoma mansoni is one of the most common etiological agents responsible for the disease schistosomiasis. More than 200 million people suffer from this disease making it the most severe tropical disease after malaria in terms of morbidity. Praziquantel (PZQ) is the treatment of choice for schistosomiasis and has been used almost exclusively to treat the disease since the 1970s. However, while the drug is lethal for sexually mature schistosomes, it is ineffective against juveniles. Thus, while morbidity can be eased, a cure is difficult to achieve. As a result there is an urgent need to develop a new generation of anti-schistosomal drugs, a task that will be made easier by understanding the mechanism of action of PZQ. As yet, neither the molecule to which PZQ binds nor the means by which it kills mature schistosomes is known. The overarching aim of this study was to understand the molecular basis of PZQ sensitivity in S. mansoni. We believe that juvenile worms survive PZQ treatment in vivo due to the induction of, as yet, unidentified protective molecular pathways. To address this hypothesis juvenile and adult PR1 S. mansoni were treated in vitro with sub-lethal concentrations of PZQ. mRNA was extracted from replicate samples, cRNA prepagreen and labeled with cyanine dyes for analysis using a 44K S. mansoni microarray. The data was then analyzed using Genespring. Our findings suggest that a number of genes associated with drug transport, iron homeostasis and apoptosis are induced in juvenile but not adult schistosomes and that this allows the juvenile worms to protect themselves against the lethal effects of PZQ long enough for the drug to be metabolized by the human host.

2011-05-27 | GSE29535 | GEO

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