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Sent on Wednesday, 2009 Nov 18Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | J Immunol. 2009 Nov 16. [Epub ahead of print]Dendritic Cells Matured by Inflammation Induce CD86-Dependent Priming of Naive CD8+ T Cells in the Absence of Their Cognate Peptide Antigen.Maroof A, Beattie L, Kirby A, Coles M, Kaye PM.Centre for Immunology and Infection, Hull York Medical School and Department of Biology, University of York, Wentworth Way, York, United Kingdom. Dendritic cells (DC) licensed by the interaction between pathogen products and pattern recognition receptors can activate naive T cells to undergo Ag-dependent proliferation and cytokine production. In contrast, DC induced to mature by trans-acting inflammatory stimuli are believed to only be capable of supporting Ag-dependent proliferative responses. In this study, we show that uninfected DC matured as a consequence of Leishmania-induced inflammation induce CD8(+) T cells to proliferate in the absence of their cognate Ag. We separated splenic DC from Leishmania donovani-infected mice into those that contained parasites and had been activated to induce IL-12p40, from those that had undergone only partial maturation, measured by increased CD86 expression in the absence of IL-12p40 induction. We then showed that these partially matured DC could induce exogenous peptide-independent proliferation of OT-I and F5 CD8(+) TCR transgenic T cells, as well as polyclonal CD8(+) T cells. Proliferation of OT-I cells was significantly inhibited in vitro and in vivo by anti-CD86 mAb but not by anti-CD80 mAb and could also be inhibited by cyclosporine A. Proliferating OT-I cells did not produce IFN-gamma, even when re-exposed to mature DC. However, these primed OT-I cells subsequently produced effector cytokines, not just on exposure to their cognate peptide but, more importantly, to weak exogenous TCR agonists that otherwise failed to induce IFN-gamma. We further showed that OT-I cells undergoing locally driven proliferation to another pathogen, Streptococcus pneumoniae, rapidly seeded other lymphoid tissues, suggesting that CD8(+) T cells primed in this way may play a role in rapidly countering pathogen dissemination. |
| PMID: 19917700 [PubMed - as supplied by publisher] | |
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| 2. | Ann Dermatol Venereol. 2009 Nov;136(11):815-6. Epub 2009 Oct 9.[Multifocal cutaneous leishmaniasis due to Leishmania infantum under adalimumab therapy.][Article in Fre nch] Schneider P, Bouaziz JD, Foulet F, Duong TA, Valeyrie Allanore L, Bagot M.Service de dermatologie, hôpital Henri-Mondor, 51, avenue du Maréchal-de-Tassigny, 94010 Créteil cedex, France. |
| PMID: 19917436 [PubMed - in process] | |
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| 3. | Eur J Pharmacol. 2009 Nov 13. [Epub ahead of print]The putative lipid raft modulator miltefosine displays immunomodulatory action in T-cell dependent dermal inflammation models.Bäumer W, Wlaź P, Jennings G, Rundfeldt C.Department of Pharmacology, Toxicology, and Pharmacy, University of Veterinary Medicine Hannover, Bünteweg 17, D-30559 Hannover, Germany. Miltefosine is currently marketed for treatment of skin metastasis of breast cancer and leishmaniasis. The mechanism of action is not fully understood, however, miltefosine is considered to be a prototype lipid raft modulator. The compound was shown to inhibited anti-IgE induced histamine release from human skin mast cell. After topical treatment it reduced skin reaction in allergic human volunteers undergoing skin prick test. The aim of this study was to test whether miltefosine could also modify T-cell signalling and whether the drug may be useful for the treatment of atopic dermatitis. Miltefosine (20microM) inhibited T-cell proliferation by >50% in the mixed lymphocyte test. In the toluene diisocyanate induced ear swelling test, miltefosine, administered topically as 2 and 6% solution or orally, attenuated ear swelling reaching 70% of the effect of dexamethasone at 100mg/kg p.o. (P<0.01). The ear tissue content of the cytokines IL1ss, IL4 and IL6 was also reduced reaching 56% or 52% reduction of IL1ss (P<0.01) after 2% topical or 100mg/kg p.o. Miltefosine significantly attenuated the allergic sensitization in the model of ovalbumin induced delayed type hypersensitivity in mice. In a model of toluene diisocyanate induced scratching a significant (P=0.0047) reduction of scratching from 47 to 6 bouts was achieved with 100mg/kg p.o. The data indicate that miltefosine modulates T-cell function in models for Th1 and Th2 related activity. This profile opens up the possibility for the treatment of T-cell related allergic diseases with a novel class of lipid raft modulator drugs such as miltefosine. |
| PMID: 19917276 [PubMed - as supplied by publisher] | |
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| 4. | BMC Genomics. 2009 Nov 16;10(1):528. [Epub ahead of print]U3 snoRNA genes are multi-copy and frequently linked to U5 snRNA genes in Euglena gracilis.Charette JM, Gray MW.ABSTRACT: BACKGROUND: U3 snoRNA is a box C/D small nucleolar RNA (snoRNA) involved in the processing events that liberate 18S rRNA from the ribosomal RNA precursor (pre-rRNA). Although U3 snoRNA is present in all eukaryotic organisms, most investigations of it have focused on fungi (particularly yeasts), animals and plants. Relatively little is known about U3 snoRNA and its gene(s) in the phylogenetically broad assemblage of protists (mostly unicellular eukaryotes). In the euglenozoon Euglena gracilis, a distant relative of the kinetoplastid protozoa, Southern analysis had previously revealed at least 13 bands hybridizing with U3 snoRNA, suggesting the existence of multiple copies of U3 snoRNA genes. RESULTS: Through screening of a lambda genomic library and PCR amplification, we recovered 14 U3 snoRNA gene variants, defined by sequence heterogeneities that are mostly located in the U3 3' -stem-loop domain. We identified three different genomic arrangements of Euglena U3 snoRNA genes: i) stand-alone, ii) linked to tRNAArg genes, and iii) linked to a U5 snRNA gene. In arrangement ii), the U3 snoRNA gene is positioned upstream of two identical tRNAArg genes that are convergently transcribed relative to the U3 gene. This scenario is reminiscent of a U3 snoRNA-tRNA gene linkage previously described in trypanosomatids. We document here twelve different U3 snoRNA-U5 snRNA gene arrangements in Euglena; in each case, the U3 gene is linked to a downstream and convergently oriented U5 gene, with the intergenic region differing in length and sequence among the variants. CONCLUSIONS: The multiple U3 snoRNA-U5 snRNA gene linkages, which cluster into distinct families based on sequence similarities within the intergenic spacer, presumably arose by genome, chromosome, and/or locus duplications. We discuss possible reasons for the existence of the unusually large number of U3 snoRNA genes in the Euglena genome. Variability in the signal intensities of the multiple Southern hybridization bands raises the possibility that Euglena contains a naturally aneuploid chromosome complement. |
| PMID: 19917113 [PubMed - as supplied by publisher] | |
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| 5. | Trop Med Int Health. 2009 Nov 16. [Epub ahead of print]Determinants of bednet ownership and use in visceral leishmaniasis-endemic areas of the Indian subcontinent.Vanlerberghe V, Singh SP, Paudel IS, Ostyn B, Picado A, Sánchez A, Rijal S, Sundar S, Davies C, Boelaert M.Epidemiology and Disease Control Unit, Department of Public Health, Institute of Tropical Medicine, Antwerp, Belgium. Objective To document ownership and use of bednets with its determinants in the visceral leishmaniasis (VL)-endemic region where mainly non-insecticide impregnated nets are available through commercial channels, and bednets are being considered as a leishmaniasis vector control measure. Methods In August-September 2006, semi-structured household (HH) questionnaires and observation guides were used in a random sample of 1330 HHs in VL-endemic districts of India and Nepal to collect data on VL knowledge, HH socio-economic status, bednet ownership and use patterns. An asset index was constructed to allow wealth ranking of the HH. A binary logistic response General Estimating Equations model was fitted to evaluate the determinants of bednet ownership and use. Results The proportion of HHs with at least one bednet purchased on the commercial market was 81.5% in India and 70.2% in Nepal. The bednets were used in all seasons by 50.6% and 54.1% of the Indian and Nepalese HH owning a bed net. There was striking inequity in bednet ownership: only 38.3% of the poorest quintile in Nepal owned at least one net, compared to 89.7% of the wealthiest quintile. In India, the same trend was observed though somewhat less pronounced (73.6%vs. 93.7%). Multivariate analysis showed that poverty was an important independent predictor for not having a bednet in the HH [OR 5.39 (2.90-10.03)]. Conclusion Given the inequity in commercial bednet ownership, free distribution of insecticide-treated bednets to the general population seems imperative to achieve a mass effect on vector density. |
| PMID: 19917036 [PubMed - as supplied by publisher] | |
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| 6. | J Med Chem. 2009 Nov 16. [Epub ahead of print]Structure-Based Design of Pteridine Reductase Inhibitors Targeting African Sleeping Sickness and the Leishmaniases.Tulloch LB, Martini VP, Iulek J, Huggan JK, Lee JH, Gibson CL, Smith TK, Suckling CJ, Hunter WN.Division of Biological Chemistry and Drug Discovery, College of Life Sciences, University of Dundee, Dundee, DD1 5EH, U.K. Pteridine reductase (PTR1) is a target for drug development against Trypanosoma and Leishmania species, parasites that cause serious tropical diseases and for which therapies are inadequate. We adopted a structure-based approach to the design of novel PTR1 inhibitors based on three molecular scaffolds. A series of compounds, most newly synthesized, were identified as inhibitors with PTR1-species specific properties explained by structural differences between the T. brucei and L. major enzymes. The most potent inhibitors target T. brucei PTR1, and two compounds displayed antiparasite activity against the bloodstream form of the parasite. PTR1 contributes to antifolate drug resistance by providing a molecular bypass of dihydrofolate reductase (DHFR) inhibition. Therefore, combining PTR1 and DHFR inhibitors might improve therapeutic efficacy. We tested two new compounds with known DHFR inhibitors. A synergistic effect was observed for one particular combination highlighting the potential of such an approach for treatment of African sleeping sickness. |
| PMID: 19916554 [PubMed - as supplied by publisher] | |
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| 7. | Am J Trop Med Hyg. 2009 Nov;81(5):900-5.Micro-positron emission tomography in the evaluation of Trypanosoma cruzi-induced heart disease: Comparison with other modalities.Prado CM, Fine EJ, Koba W, Zhao D, Rossi MA, Tanowitz HB, Jelicks LA.Department of Pathology, University of São Paulo, Ribeirão Preto, Brazil. Noninvasive assessment of cardiac structure and function is essential to understand the natural course of murine infection with Trypanosoma cruzi. Magnetic resonance imaging (MRI) and echocardiography have been used to monitor anatomy and function; positron emission tomography (PET) is ideal for monitoring metabolic events in the myocardium. Mice infected with T. cruzi (Brazil strain) were imaged 15-100 days post infection (dpi). Quantitative (18)F-FDG microPET imaging, MRI and echocardiography were performed and compared. Tracer ((18)F-FDG) uptake was significantly higher in infected mice at all days of infection, from 15 to 100 dpi. Dilatation of the right ventricular chamber was observed by MRI from 30 to 100 dpi in infected mice. Echocardiography revealed significantly reduced ejection fraction by 60 dpi. Combination of these three complementary imaging modalities makes it possible to noninvasively quantify cardiovascular function, morphology, and metabolism from the earliest days of infection through the chronic phase. |
| PMID: 19861629 [PubMed - indexed for MEDLINE] | |
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| 8. | J Med Chem. 2009 Oct 8;52(19):5793-802.Discovery of novel antileishmanial agents in an attempt to synthesize pentamidine-aplysinopsin hybrid molecule.Porwal S, Chauhan SS, Chauhan PM, Shakya N, Verma A, Gupta S.Division of Medicinal & Process Chemistry, Central Drug Research Institute, Lucknow, India. In an attempt to synthesize pentamidine-aplysinopsin hybrid molecule 25, a lead molecule 8 (containing Z-configured aplysinopsin moiety) was identified for antileishmanial activity. Optimization of lead 8 provided 24 (containing E-configured aplysinopsin) possessing 10 times more activity and 401-fold less toxicity than the drug pentamidine in cell based assays. Synthesis of 24 was possible, surprisingly, because of two innate reactivities of indole-3-carbaldehyde which provided it in diastereo- and regio-selectively pure form without recourse to the long reaction pathway. |
| PMID: 19743860 [PubMed - indexed for MEDLINE] | |
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| 9. | Bull World Health Organ. 2009 Jul;87(7):491-2.Chagas: one hundred years later.Jurberg C.PMCID: 2704045 |
| PMID: 19649360 [PubMed - indexed for MEDLINE] | |
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| 10. | Rev Biol Trop. 2009 Mar-Jun;57(1-2):13-22.[The immunosuppressant effect of T. lewisi (Kinetoplastidae) infection on the multiplication of Toxoplasma gondii (Sarcocystidae) on alveolar and peritoneal macrophages of the white rat][Article in Spanish] Carrera NJ, Carmona MC, Guerrero OM, Castillo AC.Departamento de Parasitología, Facultad de Microbiología, Universidad de Costa Rica, Costa Rica. toxogondii@gmail.com The immunosuppressant effect of T. lewisi infection on the multiplication of T. gondii was compared in peritoneal (MP) and alveolar macrophages (MA) of white rat. Two animal groups were infected with T. lewisi and sacrificed after four days and seven days post infection. A group without infection was maintained as a control. The number of intracellular parasites (tachyzoites) (IT) was counted by light microscopy, calculating the rate infection rate per 100 total cells (TC) and per infected cells (IC) for each group of phagocyte cells. The relation quotient IT, TC or IC multiplied percent, provided a statistical ratio (RE) of the relative number of parasites in both cellular types for each time interval. MA as well as MP obtained after 4 days showed a significant increase in the multiplication of T. gondii with respect to the control. Unlike the MP (which had an increase in the multiplication of T. gondii the fourth day of infection with T. lewisi diminishing towards the seventh day), the MA had an increase in the multiplication of the parasite from the fourth to the seventh day. This difference can be related to the route of infection used for the experiments, that affect the MP directly with a greater effect in comparison with the MA of the lungs. Lung compartment will be affected later, when the infection becomes systemic between the fourth and sixth day of infection. The immunity against T. gondii is similar between both phagocytes, but the time of infection and the compartment where the cells are located, makes the difference in the response time against T. gondii. Supernatants from macrophage cultures or T. lewisi by rat did not induced any immunosuppression. |
| PMID: 19637684 [PubMed - indexed for MEDLINE] | |
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