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Sent on Friday, 2011 Sep 02Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | Arch Dermatol Res. 2011 Sep 1. [Epub ahead of print]Analysis of the protective potential of antigens released by Leishmania (Viannia) shawi promastigotes.Passero LF, Marques C, Vale-Gato I, Corbett CE, Laurenti MD, Santos-Gomes G.SourceLaboratório de Patologia de Moléstias Infecciosas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil. AbstractLeishmania (Viannia) shawi causes cutaneous lesions in humans. Parasite antigens conferring significant protection against American tegumentar leishmaniosis (ATL) might be important for the development of effective vaccine. Therefore, this work evaluates the protective effect of antigenic fractions released by L. shawi. Antigens released by promastigotes to culture medium were concentrated and isolated by SDS-PAGE. The three main fractions LsPass1 (>75 kDa), LsPass2 (75-50 kDa) and LsPass3 (<50 kDa) were electro-eluted according with their molecular mass. Immunized BALB/c mice were challenged with L. shawi promastigotes and the course of infection monitored during 5 weeks. LsPass1-challenged mice showed no protection, however, a strong degree of protection associated to smaller lesions and high expression of IFN-γ and TNF-α by CD4(+) T, CD8(+) T and double negative CD4CD8 cells was achieved in LsPass3-challenged mice. Furthermore, LsPass2-challenged mice showed an intermediated degree of protection associated to high levels of IFN-γ, IL-4 and IL-10 mRNA. In spite of increased expression of IFN-γ and TNF-α, high amounts of IL-4 and IL-10 mRNA were also detected in LsPass3-challenged mice indicating a possible contribution of these cytokines for the persistence of a residual number of parasites that may be important in inducing long-lasting immunity. Therefore, LsPass3 seems to be an interesting alternative that should be considered in the development of an effective vaccine against ATL. |
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| 2. | Cell Death Dis. 2011 Sep 1;2:e201. doi: 10.1038/cddis.2011.83.Tolerance to drug-induced cell death favours the acquisition of multidrug resistance in Leishmania.Moreira W, Leprohon P, Ouellette M.SourceCentre de Recherche en Infectiologie du CHUL, Université Laval, Québec, Quebec, Canada. AbstractThe control of the protozoan parasite Leishmania relies on few drugs with unknown cellular targets and unclear mode of action. Several antileishmanials, however, were shown to induce apoptosis in Leishmania and this death mechanism was further studied in drug-sensitive and drug-resistant Leishmania infantum. In sensitive parasites, antimonials (SbIII), miltefosine (MF) and amphotericin B (AMB), but not paromomycin (PARO), triggered apoptotic cell death associated with reactive oxygen species (ROS). In contrast, Leishmania mutants resistant to SbIII, MF or AMB not only failed to undergo apoptosis following exposure to their respective drugs, but also were more tolerant towards apoptosis induced by other antileishmanials, provided that these killed Leishmania via ROS production. Such tolerance favored the rapid acquisition of multidrug resistance. PARO killed Leishmania in a non-apoptotic manner and failed to produce ROS. PARO resistance neither protected against drug-induced apoptosis nor provided an increased rate of acquisition of resistance to other antileishmanials. However, the PARO-resistant mutant, but not SbIII-, MF- or AMB-resistant mutants, became rapidly cross-resistant to methotrexate, a model drug also not producing ROS. Our results therefore link the mode of killing of drugs to tolerance to cell death and to a facilitated emergence of multidrug resistance. These findings may have fundamental implications in the field of chemotherapeutic interventions. |
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| 3. | J Infect Dis. 2011 Oct;204(7):1134-7.IL-10 neutral ization promotes parasite clearance in splenic aspirate cells from patients with visceral leishmaniasis.Gautam S, Kumar R, Maurya R, Nylén S, Ansari N, Rai M, Sundar S, Sacks D.SourceDepartment of Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi. AbstractThe mechanisms underlying the failure to contain the growth of Leishmania parasites in human visceral leishmaniasis (VL) are not understood. L donovani amastigotes were quantified in cultured splenic aspirate cells to assess the function of IL-10 in lesional tissue ex vivo. In 67 patients with active VL, IL-10 neutralization promoted parasite killing in 73% and complete clearance in 30%, while 18% had more parasites and 9% did not change. The splenic cells secreted increased levels of both tumor necrosis factor α (TNFα) and interferon γ (IFNγ) under IL-10-neutralizing conditions. These findings provide direct support for targeting IL-10 as an approach to therapy in human VL. |
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| 4. | Clin Vaccine Immunol. 2011 Aug 31. [Epub ahead of print]EVALUATION OF A RECOMBINANT TRYPANOSOMA CRUZI MUCIN-LIKE ANTIGEN FOR SERODIAGNOSIS OF CHAGAS DISEASE.De Marchi CR, Di Noia JM, Frasch AC, Amato Neto V, Almeida IC, Buscaglia CA.SourceDepartamento de Parasitologia, Instituto de Ciências Biomédicas, Universidade de São Paulo (ICM-USP), São Paulo, Brazil. AbstractChagas disease is caused by the protozoan parasite Trypanosoma cruzi and is one of the most important endemic problems in Latin America. Lately, it has also become a health concern to the U.S. and Europe. Current diagnosis of Chagas disease and the screening of blood supplies for anti-parasite antibodies are achieved by conventional serological tests that show substantial variation in their reproducibility and reliability. In addition, the specificity of these assays is curtailed by antigenic cross-reactivity with sera from patients affected by other endemic diseases such as leishmaniasis. Here we used a highly sensitive chemiluminescent ELISA (CL-ELISA) to evaluate a recombinant protein core of a mucin-like molecule (termed TSSA) for the detection of specific serum antibodies in a broad panel of human sera. The same samples were evaluated by CL-ELISA using as antigen either a mixture of native T. cruzi trypomastigote mucins or an epimastigote extract and, for further comparison, by conventional serologic tests such as indirect hemmagglutination assay and indirect immunofluorescence assay. TSSA showed ∼87% sensitivity among the seropositive Chagasic panel, a value which was increased up to >98% when only parasitological positive samples were considered. More importantly, TSSA shows a significant increase in specificity (97.4%) when compared to currently used assays, which averaged 80-90%. Overall, our data demonstrate that recombinant TSSA may be a useful antigen for the immunodiagnosis of Chagas disease. |
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| 5. | J Biol Chem. 2011 Aug 31. [Epub ahead of print]Adaptor protein-3 (AP-3) complex mediates the biogenesis of acidocalcisomes and is essential for growth and virulence of Trypanosoma brucei.Huang G, Fang J, Sant'anna C, Li Z, Wellems DL, Rohloff P, Docampo R.SourceUniversity of Georgia, United States. AbstractAcidocalcisomes are acidic calcium- and polyphosphate-storage organelles found in a diverse range of organisms. Here we present evidence that the biogenesis of acidocalcisomes in Trypanosoma brucei is linked to the expression of adaptor protein-3 complex (AP-3). Localization studies in cell lines expressing β3 and δ subunits of AP-3 fused to epitope tags revealed their partial co-localization with the vacuolar proton pyrophosphatase (VP1), a marker of acidocalcisomes, with the Golgi marker Golgi reassembly and stacking protein (GRASP), and with antibodies against the small GTPase Rab11. Ablation of the β3 subunit by RNA interference (RNAi) resulted in disappearance of acidocalcisomes from both procyclic (PCF) and bloodstream form (BSF) trypanosomes, as revealed by immmunofluorescence and electron microscopy assays, with no alterations in trafficking of different markers to lysosomes. Knockdown of the β3 subunit resulted in lower acidic calcium, pyrophosphate and polyphosphate content, as well as defects in growth in culture, resistance to osmotic stress, and virulence in mice. Similar results were obtained by knocking down the expression of the δ subunit of AP-3. These results indicate that AP-3 is essential for the biogenesis of acidocalcisomes, and for growth and virulence of T. brucei. |
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| 6. | Vet Parasitol. 2011 Aug 4. [Epub ahead of print]Axenic culture and identification of amastigotes from Sichuan human strain of Chinese Leishmania isolates.Cao DP, Chen DL, Chen JP, Liao L, Yang BB, Hu XS.SourceDepartment of Parasitology, West China School of Preclinical and Forensic Medicine, Sichuan University, No. 17 Section 3, Renmin South Road, Chengdu 610041, Sichuan, China. AbstractThis work describes a simple method to yield large amounts of the isolate MHOM/CN/90/SC10H2 amastigotes-like forms in axenic cultures using promastigotes as the starting population. The isolate MHOM/CN/90/SC10H2, used in this study, belongs to an undescribed species of Leishmania endemic to hill foci in China. The method describes induced extracellular amastigote transformation of this isolate. The rounded parasite obtained in axenic culture was morphologically similar, even at the ultrastructural level, to intracellular amastigotes. Moreover, the axenic amastigotes remained viable as verified by the stage-specific genes (gp46 and p4 genes) with RT-PCR. A 70-80kDa protein was recognized by polyclonal antibody HRP-IgG only in axenic-derived amastigotes and not in promastigotes. Copyright © 2011 Elsevier B.V. All rights reserved. |
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| 7. | Future Med Chem. 2011 Sep;3(11):1361-71.Drugs for Neglected Diseases initiative model of drug development for neglected diseases: current status and future challenges.Ioset JR, Chang S.SourceDrugs for Neglected Diseases initiative (DNDi), 15 Chemin Louis-Dunant, 1202 Geneva, Switzerland. AbstractThe Drugs for Neglected Diseases initiative (DNDi) is a patients' needs-driven organization committed to the development of new treatments for neglected diseases. Created in 2003, DNDi has delivered four improved treatments for malaria, sleeping sickness and visceral leishmaniasis. A main DNDi challenge is to build a solid R&D portfolio for neglected diseases and to deliver preclinical candidates in a timely manner using an original model based on partnership. To address this challenge DNDi has remodeled its discovery activities from a project-based academic-bound network to a fully integrated process-oriented platform in close collaboration with pharmaceutical companies. This discovery platform relies on dedicated screening capacity and lead-optimization consortia supported by a pragmatic, structured and pharmaceutical-focused compound sourcing strategy. |
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| 8. | Blood. 2011 Jul 7;118(1):8.Leishman-Donovan bodies in the bone marrow biopsy.Bibas M, Del Nonno F.SourceNational Institute for Infectious Diseases, Rome, Italy. |
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| 9. | PLoS One. 2011 Feb 14;6(2):e16977.Evidence for a role of the host-specific flea (Paraceras melis) in the transmission of Trypanosoma (Megatrypanum) pestanai to the European badger.Lizundia R, Newman C, Buesching CD, Ngugi D, Blake D, Sin YW, Macdonald DW, Wilson A, McKeever D.SourceRoyal Veterinary College, University of London, Hatfield, United Kingdom. AbstractWe investigated the epidemiology of Trypanosoma pestanai infection in European badgers (Meles meles) from Wytham Woods (Oxfordshire, UK) to determine prevalence rates and to identify the arthropod vector responsible for transmission. A total of 245 badger blood samples was collected during September and November 2009 and examined by PCR using primers derived from the 18S rRNA of T. pestanai. The parasite was detected in blood from 31% of individuals tested. T. pestanai was isolated from primary cultures of Wytham badger peripheral blood mononuclear cells and propagated continually in vitro. This population was compared with cultures of two geographically distinct isolates of the parasite by amplified fragment length polymorphism (AFLP) and PCR analysis of 18S rDNA and ITS1 sequences. High levels of genotypic polymorphism were observed between the isolates. PCR analysis of badger fleas (Paraceras melis) collected from infected individuals at Wytham indicated the presence of T. pestanai and this was confirmed by examination of dissected specimens. Wet smears and Giemsa-stained preparations from dissected fleas revealed large numbers of trypanosome-like forms in the hindgut, some of which were undergoing binary fission. We conclude that P. melis is the primary vector of T. pestanai in European badgers. |
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