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
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
Project description:Transcriptional profiling using two subsequent developmental stages of Schistosoma mansoni (Egg vs. Miracidium; Cercaria vs. 7-days-old Schistosomulum; 7-days-old Schistosomulum vs. Adult worms