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182 results for “leishmania”
Fig. 1 in Molecular detection and characterization of Leishmania infantum in free- ranging Egyptian mongoose (Herpestes ichneumon)
Fig. 1. Spatial distribution of wild carnivore samples in mainland Portugal. Administrative regions at the district level are indicated. The overall proportion of samples per district is indicated by the grey scale. The abbreviatures of districts are as follows: Viana do Castelo (VC), Braga (BR), Vila Real (VR), Bragança (BG), Porto (PT), Aveiro (AV) Viseu (VS), Guarda (GR), Coimbra (CM), Castelo Branco (CB), Leiria (LR), Santarém (SA), Portalegre (PA), Lisboa (Lx), Setúbal (ST), Évora (EV), Beja (BJ) and Faro (FR). White circles with numbers in red specify the number and location of Egyptian mongooses that were kDNA-positive by PCR. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 4 in Leishmania presence in bats in areas endemic for leishmaniasis in centralwest Brazil
Fig. 4. Identification of Leishmania according to site of collect of the bats per city, Mato Grosso do Sul, Brazil; Grey area - municipal boundary; A – Campo Grande; B – Corumbá; C – Ivinhema; D – Brasilândia.
Fig. 3 in Leishmania presence in bats in areas endemic for leishmaniasis in centralwest Brazil
Fig. 3. Agarose gel demonstrating LnPCR products (350bp). M: 100bp marker, 1–17: analyzed samples, of which 2, 7, 10 and 14 were considered positive. PC: positive control of Leishmania spp., NC: negative control.
Fig. 4 in Utilising a novel surveillance system to investigate species of Forcipomyia (Lasiohelea) (Diptera: Ceratopogonidae) as the suspected vectors of Leishmania macropodum (Kinetoplastida: Trypanosomatidae) in the Darwin region of Australia
Fig. 4. Assessment of L. macropodum DNA using FTAṜ card technology. FTAṜ cards were exposed to field-collected F. (Lasiohelea). Cards with and without insects adhered were processed and parasite load was determined with qPCR. 4.83% (7/145) FTAṜ cards were positive for L. macropodum DNA. Black columns show parasite load detected on each positive FTAṜ card (numbered FTA.1 – FTA.7). Dashed columns show the number of insects adhered to each card. When dashed columns are absent, this signifies the absence of insects on the positive cards.
Fig. 1 in Utilising a novel surveillance system to investigate species of Forcipomyia (Lasiohelea) (Diptera: Ceratopogonidae) as the suspected vectors of Leishmania macropodum (Kinetoplastida: Trypanosomatidae) in the Darwin region of Australia
Fig. 1. Wax-paper cups were used to contain and maintain field-collected biting midges. (A) Honey-coated FTAṜ cards were left at room temperature for 48 h allowing even absorption of honey into the cards. (B) A 2.5 cm slit was carved into the bottom of disposable cup and sealed with adhesive tape. (C) Insects were aspirated directly into the bottom of the containers through a small perforation created before field collection. Once biting midges were collected from the macropods, the small perforation was sealed with a rubber plug. Gauze was used as a lid to seal the top of the containers and fastened securely with a rubber band. The honey-coated FTAṜ card was inserted through the bottom slit after insect collection and once again sealed with adhesive tape.
Fig. 2 in Utilising a novel surveillance system to investigate species of Forcipomyia (Lasiohelea) (Diptera: Ceratopogonidae) as the suspected vectors of Leishmania macropodum (Kinetoplastida: Trypanosomatidae) in the Darwin region of Australia
Fig. 2. Leishmania macropodum DNA detection by qPCR. Individual or pools of F. (Lasiohelea) species were assessed for the presence of L. macropodum DNA. Only positive samples are shown, with each pair of columns representing results from one sample. Black columns depict the parasitic load detected and the dashed columns show the number of insects processed in that sample. Asterisks represent groups that contained ≥ 5 × 106 F. (Lasiohelea) parasites.
Fig. 3 in Host competence of Algerian Gerbillus amoenus for Leishmania major
Fig. 3. The external manifestation of L. major infection in Gerbillus amoenus. A) non-infected ear, B) 8th-week post-infection, C) 11th-week post-infection, D) 6 months post-infection.
Fig. 2 in Host competence of Algerian Gerbillus amoenus for Leishmania major
Fig. 2. Lesion growth in Gerbillus amoenus and Balb/c mice. Data are presented as the means ± standard errors of the means.
Data sets for de Oliveira et al.: "Leishmania major telomerase RNA knockout: from altered cell proliferation to decreased parasite infectivity"
<p><strong><span>This file contains relevant data about the article: "</span></strong><em><span>Leishmania major</span></em><strong><span> telomerase RNA knockout: from altered cell proliferation to decreased parasite infectivity"</span></strong></p>
Data sets for Shiburah et al., "The absence of the Leishmania major telomerase TERT component links telomeres and cell homeostasis with infectivity"
<p>These files correspond to the figures and information contained in Shiburah et al., "The absence of the <em>Leishmania major</em> telomerase TERT component links telomeres and cell homeostasis with infectivity"</p>
"Síntesis de hemo en el ciclo de vida de Leishmania, un parásito auxótrofo para este metabolito esencial"
<p>El hemo es una molécula esencial para los organismos aerobios al participar como cofactor de hemoproteínas indispensables para el metabolismo celular. Casi todos los organismos lo sintetizan a partir de una ruta biosintética muy conservada formada por ocho pasos. Una excepción la constituyen los parásitos tripanosomátidos <em>Leishmania</em>, <em>Trypanosoma brucei</em> y <em>Trypanosoma cruzi</em>, responsables de la leishmaniosis, la enfermedad del sueño y la enfermedad de Chagas, respectivamente. Aunque estos protozoos necesitan el hemo, han perdido su ruta de síntesis durante la evolución, por lo que son auxótrofos para este metabolito y necesitan captarlo del hospedador infectado. A diferencia de <em>Trypanosoma</em>, <em>Leishmania</em> recuperó los genes que codifican las tres últimas enzimas de la ruta (CPOX, PPOX y FeCH) mediante transferencia horizontal a partir de proteobacterias. La presencia de estos genes es enigmática ya que el parásito no puede sintetizar los precursores sustrato. Si estos genes readquiridos fueran indispensables para el parásito los convertiría en prometedores blancos terapéuticos. Además, su origen bacteriano hace que tengan una baja similitud de secuencia con sus homólogos humanos, lo que supone una ventaja para la identificación de inhibidores específicos. El objetivo del presente trabajo fue caracterizar la ruta de síntesis de hemo de <em>Leishmania major</em> y estudiar su potencialidad como blanco terapéutico. Para ello, en primer lugar, comprobamos que los parásitos intracelulares eran capaces de usar porfirinas preformadas por el macrófago para sintetizar hemo. Además, demostramos la actividad de la CPOX, PPOX y FeCH de <em>L. major</em> mediante ensayos de complementación funcional utilizando levaduras y bacterias mutantes carentes de las enzimas ortólogas. De manera interesante, mostramos que la actividad de enzima PPOX de <em>L. major</em> no se afecta por inhibidores de la PPOX eucariota, lo que confirma la posibilidad de inhibir específicamente las proteínas del parásito. El marcaje <em>in situ</em> con etiquetas fluorescentes mostró que las enzimas PPOX y FeCH se localizan en la mitocondria del parásito, mientras que la enzima CPOX es una proteína citosólica. Para determinar la esencialidad de estas proteínas, se generaron parásitos knockout para cada gen mediante CRISPR-Cas9. En las formas promastigotas, la deleción del gen <em>fech</em> no alteró el crecimiento <em>in vitro</em> ni impidió el desarrollo <em>in vivo</em> del parásito en el insecto vector. Por el contrario, sí disminuyó la capacidad de los amastigotes intracelulares para replicarse dentro del macrófago. Sin embargo, usando un modelo murino de leishmaniasis cutánea, los parásitos FeCH<sup>-/-</sup> presentaron la misma virulencia que los parásitos controles. Estos resultados sugieren que, aunque los parásitos son capaces de sintetizar hemo a partir de porfirinas preformadas por el macrófago, esta actividad no es esencial <em>in vivo</em>, probablemente porque el parásito es capaz de tomar hemo de otras fuentes. Sin embargo, no descartamos que la biosíntesis de hemo en <em>Leishmania</em> pueda desempeñar un papel crucial en el desarrollo del parásito en condiciones naturales, afectando su virulencia o potencial de transmisión. En futuros trabajos queremos estudiar el papel de la síntesis de hemo en <em>Leishmania</em> en condiciones naturales de infección y también la importancia de esta ruta en especies causantes de leishmaniasis visceral.</p>
SINTESIS DE HEMO EN EL CICLO DE VIDA DE Leishmania, UN PARASITO AUXÓTROFO PARA ESTE METABOLITO ESENCIAL
<p><strong>El hemo es una molécula esencial para los organismos aerobios al participar como cofactor de hemoproteínas indispensables para el metabolismo celular. Casi todos los organismos lo sintetizan a partir de una ruta biosintética muy conservada formada por ocho pasos. Una excepción la constituyen los parásitos tripanosomátidos Leishmania, Trypanosoma brucei y Trypanosoma cruzi, responsables de la leishmaniosis, la enfermedad del sueño y la enfermedad de Chagas, respectivamente. Aunque estos protozoos necesitan el hemo, han perdido su ruta de síntesis durante la evolución, por lo que son auxótrofos para este metabolito y necesitan captarlo del hospedador infectado. A diferencia de Trypanosoma, Leishmania recuperó los genes que codifican las tres últimas enzimas de la ruta (CPOX, PPOX y FeCH) mediante transferencia horizontal a partir de proteobacterias. La presencia de estos genes es enigmática ya que el parásito no puede sintetizar los precursores sustrato. Si estos genes readquiridos fueran indispensables para el parásito los convertiría en prometedores blancos terapéuticos. Además, su origen bacteriano hace que tengan una baja similitud de secuencia con sus homólogos humanos, lo que supone una ventaja para la identificación de inhibidores específicos. El objetivo del presente trabajo fue caracterizar la ruta de síntesis de hemo de Leishmania major y estudiar su potencialidad como blanco terapéutico. Para ello, en primer lugar, comprobamos que los parásitos intracelulares eran capaces de usar porfirinas preformadas por el macrófago para sintetizar hemo. Además, demostramos la actividad de la CPOX, PPOX y FeCH de L. major mediante ensayos de complementación funcional utilizando levaduras y bacterias mutantes carentes de las enzimas ortólogas. De manera interesante, mostramos que la actividad de enzima PPOX de L. major no se afecta por inhibidores de la PPOX eucariota, lo que confirma la posibilidad de inhibir específicamente las proteínas del parásito. El marcaje in situ con etiquetas fluorescentes mostró que las enzimas PPOX y FeCH se localizan en la mitocondria del parásito, mientras que la enzima CPOX es una proteína citosólica. Para determinar la esencialidad de estas proteínas, se generaron parásitos knockout para cada gen mediante CRISPR-Cas9. En las formas promastigotas, la deleción del gen fech no alteró el crecimiento in vitro ni impidió el desarrollo in vivo del parásito en el insecto vector. Por el contrario, sí disminuyó la capacidad de los amastigotes intracelulares para replicarse dentro del macrófago. Sin embargo, usando un modelo murino de leishmaniasis cutánea, los parásitos FeCH-/- presentaron la misma virulencia que los parásitos controles. Estos resultados sugieren que, aunque los parásitos son capaces de sintetizar hemo a partir de porfirinas preformadas por el macrófago, esta actividad no es esencial in vivo, probablemente porque el parásito es capaz de tomar hemo de otras fuentes. Sin embargo, no descartamos que la biosíntesis de hemo en Leishmania pueda desempeñar un papel crucial en el desarrollo del parásito en condiciones naturales, afectando su virulencia o potencial de transmisión. En futuros trabajos queremos estudiar el papel de la síntesis de hemo en Leishmania en condiciones naturales de infección y también la importancia de esta ruta en especies causantes de leishmaniasis visceral</strong></p>
Fig. 1 in Characterization of Leishmania spp. causing cutaneous leishmaniasis in Manaus, Amazonas, Brazil
Fig. 1 Locations of case occurrence in Manaus and its metropolitan regions
Fig. 1 in Host competence of Algerian Gerbillus amoenus for Leishmania major
Fig. 1. Location map of the study area.
Characterization and cellular localization of a SFT-2/Got-1- like transporter protein of Leishmania infantum
<p><strong>Abstract</strong>: Background: Visceral leishmaniasis affects approximately 12 million people worldwide. Current existing drugs cause several side effects and resistance, the identification of new therapeutic targets for the development of new drugs is necessary. The vesicular trafficking in the parasite flagellar pocket is essential for parasite survival and proliferation, but little is known about the proteins involved in the endocytic/secretory pathways. In this work, we are describing the characterization of a transporter cargo protein SFT-2/Got-1 like in <em>Leishmania infantum</em>. <strong>Material and Methods:</strong> Using bioinformatics tools, the putative Got-1 protein A4HSK3 was characterized structurally and phylogenetically. Molecular biology was used to clone and express the protein and confocal fluorescence to determine its subcellular localization. <strong>Results:</strong> The Got-1 like protein presents four alpha helix TM conserved domains (aa38-aa147) characteristics of the Got-1/SFT-2 family proteins and an important PEN-2 conserved motif LGDYXXF located in the extracellular loop. Confocal microscopy suggests that Got-1/SFT-2 like is localized in the flagellar pocket, and is partially co-localized with the <em>L. infantum</em> presenilin-like protein. Phylogenetically, the <em>Leishmania sp</em> Got-1 like is contained in a subgroup of proteins clearly detached from the other Trypanosomatidae, such as <em>T. cruzi</em> and <em>T. brucei</em>. <strong>Conclusions:</strong> Our data show the presence of an important transported proteins, and its colocalizatoin with the presenilin aspartyl protease in the flagelar pocket of the <em>L. infantum</em> open new perspectives to identify novel targets, which can be an alternative therapeutic strategy against leishmaniasis</p>
Leishmanicidal and healing effects of 3β,6β,16β-trihydroxy lup-20 (29)-ene isolated from Combretum leprosum on Leishmania braziliensis infection in vitro and in vivo
<p>Treatment of cutaneous leishmaniasis depends on drugs that potentially cause serious side effects and resistance. Thus, topical therapies are attractive alternatives to the drugs currently used. 3β, 6β, 16β-trihydroxylup-20 (29)-ene is a lupane triterpene isolated from Combretum leprosum Mart. leaves (CLF-1), with reports of in vitro antileishmanial effect against L. amazonensis and to promote lesion healing in animal model. Herein, we evaluated the in vitro and in vivo antileishmanial and healing effects of CLF-1 against L. braziliensis. CLF-1 treatment showed low toxicity in macrophages and significantly reduced parasite load in vitro. CLF-1 induced higher IL-12 and TNF-α production and more discrete IL-4 and IL-10 production. For in vivo evaluation, a CLF-1 cream formulation was prepared to treat hamsters infected with L. braziliensis. CLF-1 treatment was able to reduce parasite load on the infected skin and lymph node more efficiently than the conventional treatment. Histopathological analysis indicated a strong inflammatory response accompanied by an important healing response. Data from this study indicate that topical CLF-1 treatment was effective and non-toxic in L. braziliensis infected hamsters suggesting its potential for further development as a future therapeutic intervention.</p>
Data from: Unraveling the biochemical aspects of the interaction between ticks and <em>Leishmania</em> using a tick cell line
Open the record for dataset details and reuse information.
Pathway/Genome Database (PGDB) for Leishmania major, Leishmania infantum, Leishmania donovani, and Leishmania braziliensis
<p>This set of four metabolic reconstructions were created using Pathway Tools v. 18.0 and reported in the work "High-throughput prioritization of target proteins for development of new antileishmanial compounds" (under review). The methodology for automatic creation and curation is presented below.</p> <p> </p> <p> </p>
Supplementary Table S1 and Supplementary Table S2 - Part of "Next generation leishmanization: revisiting molecular targets for selecting genetically engineered live-attenuated Leishmania"
<p>Supplementary Table S1 and Supplementary Table S2 -</p> <p>Part of "Next generation leishmanization: revisiting molecular targets for selecting genetically engineered live-attenuated Leishmania"</p>
A Clinical Study to Develop a Controlled Human Infection Model Using Leishmania Major-infected Sand Flies
ClinicalTrials.gov study NCT04512742. IPD Sharing: NO. Countries: 1. Publications: 2.
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