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Sent on Saturday, 2010 Jan 23Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | Methods Mol Biol. 2010;618:393-420.Characterization of the leishmanicidal activity of antimicrobial peptides.Luque-Ortega JR, Rivas L.Centro de Investigaciones Biológicas (CSIC), Madrid, Spain. This chapter describes the basic methodology to assay the activity of antimicrobial peptides (AMPs) on Leishmania, a human protozoan parasite. The protocols included can be methodologically divided into two major blocks. The first one addresses the basic technology for growth of the different stages of Leishmania, assessment of leishmanicidal activity, and monitoring of plasma membrane permeabilization. The second block encompasses the monitoring of bioenergetic parameters of the parasite, visualization of structural damage by transmission electron microscopy, or those methods more closely related to the involvement of intracellular AMP targets, as subcellular localization of the peptide and induction of parasite apoptosis. |
| PMID: 20094878 [PubMed - in process] | |
| 2. | Vaccine. 2010 Jan 18. [Epub ahead of print]Enhanced efficacy and immunogenicity of 78kDa antigen formulated in various adjuvants against murine visceral leishmaniasis.Nagill R, Kaur S.Parasitology Laboratory, Department of Zoology, Panjab University, Chandigarh-160014, India. Leishmania infection causes localized cutaneous to severe visceral disease in humans and animals. Current control measures, based on antimonial compounds, are not effective because of resistance in Leishmania. Vaccination would be a feasible alternative, but as yet no vaccine to protect humans against infection has been commercialized. Parasite antigens that preferentially stimulate the induction of significant protection through Th1 response presents a rational approach for a vaccine against leishmaniasis. With this view in mind, we investigated the potential of 78kDa antigen of Leishmania donovani alone and along with different adjuvants against murine visceral leishmaniasis. Various adjuvants used along with 78kDa antigen include monophosphoryl lipid A (MPL-A), liposomal encapsulation, recombinant IL-12, autoclaved Leishmania antigen (ALD) and Freund's adjuvant (FCA). BALB/c mice were immunized subcutaneously thrice with respective vaccine formulation. Challenge infection was given intracardially after 2 weeks of second booster. A significant decrease in parasite burden was seen in vaccines over the infected controls on all post challenge days and was found that maximum protection was provided by 78kDa+rIL-12 vaccine and it was highly immunogenic as depicted by the reduction in parasite load (71-94.8%), reduction in infection rate of peritoneal macrophages (92.9-98%), enhanced DTH response (6.5-10.5 fold), increase in IgG2a anti-leishmanial antibody production (3-3.7 fold) and up-regulation of IFN-gamma (3.7-6.5 fold) and IL-2 levels (7.7-12.3 fold), which demonstrate the generation of protective Th1 type of immune response. Comparable results were also observed in 78kDa+MPL-A and liposome-encapsulated 78kDa vaccines with 56.5-92% and 62.9-93.4% reduction in parasite load respectively. Significant results have also been obtained with 78kDa antigen+ALD, 78kDa antigen+FCA and 78kDa antigen alone group but the protective efficacy was reduced as compared to the other vaccine groups. The present study indicates that the three vaccine formulations i.e. 78kDa antigen+rIL-12, liposome-encapsulated 78kDa antigen and 78kDa antigen+MPL-A, are highly efficacious and effective vaccine candidates against visceral leishmaniasis. Copyright © 2010. Published by Elsevier Ltd. |
| PMID: 20093205 [PubMed - as supplied by publisher] | |
| 3. | J Proteome Res. 2010 Jan 22. [Epub ahead of print]Integrated Cytokine and Metabolic Analysis of Pathological Responses to Parasite Exposure in Rodents.Saric J, Li JV, Swann J, Utzinger J, Calvert G, Nicholson JK, Dirnhofer S, Dallman M, Bictash M, Holmes E.Parasitic infections cause a myriad of responses in their mammalian hosts, including a range of immune reactions and metabolic perturbations. Here, a multiplex panel of cytokines and metabolites derived from four parasite-rodent models, namely Plasmodium berghei-mouse, Trypanosoma brucei brucei-mouse, Schistosoma mansoni-mouse and Fasciola hepatica-rat were statistically co-analyzed. 1H NMR spectroscopy and multivariate statistical analysis were used to characterize the urine and plasma metabolite profiles in infected and non-infected control animals. Each parasite generated a unique metabolic signature in the host. Plasma cytokine concentrations were obtained using the Meso Scale Discovery multi cytokine assay platform. Multivariate data integration methods were subsequently used to elucidate the component of the metabolic signature which is associated with inflammation and to determine specific metabolic correlates with parasite-induced changes in plasma cytokine levels. For example, plasma levels of acetyl glycoproteins extracted from the plasma metabolite profile in the P. berghei-infected mice were statistically correlated with IFN-gamma, whereas the same cytokine was anti-correlated with glucose levels. Both the metabolic and the cytokine data showed a similar spatial distribution in principal component analysis scores plots constructed for the combined murine data, with samples from all infected animals clustering according to the parasite species and whereby the protozoan infections grouped separately from the helminth infection. For S. mansoni, the main infection-responsive cytokines were IL-4 and IL-5, which co-varied with lactate, choline and 3-D-hydroxybutyrate. This study demonstrates that the inherently differential immune response to single- and multi-cellular parasites manifests not only in the cytokine expression, but also consequently imprints on the metabolic signature, and calls for in-depth analysis to further explore direct links between immune features and biochemical pathways. |
| PMID: 20092362 [PubMed - as supplied by publisher] | |
| 4. | Int J Parasitol. 2009 Apr;39(5):615-23. Epub 2008 Nov 17.Trypanosoma cruzi in Brazilian Amazonia: Lineages TCI and TCIIa in wild primates, Rhodnius spp. and in humans with Chagas disease associated with oral transmission.Marcili A, Valente VC, Valente SA, Junqueira AC, da Silva FM, Pinto AY, Naiff RD, Campaner M, Coura JR, Camargo EP, Miles MA, Teixeira MM.Departamento de Parasitologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, 05508-900 São Paulo, SP, Brazil. In this study, we provide phylogenetic and biogeographic evidence that the Trypanosoma cruzi lineages T. cruzi I (TCI) and T. cruzi IIa (TCIIa) circulate amongst non-human primates in Brazilian Amazonia, and are transmitted by Rhodnius species in overlapping arboreal transmission cycles, sporadically infecting humans. TCI presented higher prevalence rates, and no lineages other than TCI and TCIIa were found in this study in wild monkeys and Rhodnius from the Amazonian region. We characterised TCI and TCIIa from wild primates (16 TCI and five TCIIa), Rhodnius spp. (13 TCI and nine TCIIa), and humans with Chagas disease associated with oral transmission (14 TCI and five TCIIa) in Brazilian Amazonia. To our knowledge, TCIIa had not been associated with wild monkeys until now. Polymorphisms of ssrDNA, cytochrome b gene sequences and randomly amplified polymorphic DNA (RAPD) patterns clearly separated TCIIa from TCIIb-e and TCI lineages, and disclosed small intra-lineage polymorphisms amongst isolates from Amazonia. These data are important in understanding the complexity of the transmission cycles, genetic structure, and evolutionary history of T. cruzi populations circulating in Amazonia, and they contribute to both the unravelling of human infection routes and the pathological peculiarities of Chagas disease in this region. |
| PMID: 19041313 [PubMed - indexed for MEDLINE] | |
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| 5. | Int J Parasitol. 2009 Apr;39(5):525-32. Epub 2008 Oct 14.One- and two-hybrid analysis of the interactions between components of the Trypanosoma cruzi spliced leader RNA gene promoter binding complex.Cribb P, Serra E.Instituto de Biología Molecular y Celular de Rosario (IBR-CONICET), Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, Suipacha 531, Rosario, CP2000, Santa Fe, Argentina. The spliced leader (SL) RNA gene promoter is the only RNA polymerase II-dependent promoter characterized to date in trypanosomatids. Transcription of this small nuclear RNA is critical for trypanosomatid cell life because it is needed for polycistronic primary transcripts processing into individual translatable mRNAs. In recent years, a set of divergent fundamental transcription factors required for SL RNA gene transcription have been identified in different trypanosomatids. By means of a yeast two-hybrid system, we analyzed the protein-protein interactions between components of the SL RNA gene promoter binding complex. We also studied the interactions of already described motifs of TATA-binding protein (TBP) and transcription factor II B (TFIIB) orthologs separately. This was followed by investigations of DNA-protein interactions within the SL RNA gene promoter binding complex using one-hybrid analysis. Our results suggest that the complex has two "cores" which contact the promoter DNA, trypanosomal small nuclear RNA activating protein complex (tSNAPc), which has strong interactions between its subunits and a more labile TBP-TFIIA sub-complex. |
| PMID: 18957295 [PubMed - indexed for MEDLINE] | |
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