What's new for 'Trypanosomatids' in PubMed

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Sent on Tuesday, 2012 June 12
Search: kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"

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PubMed Results

Items 1 - 10 of 13

1.	PLoS One. 2012;7(6):e38385. Epub 2012 Jun 7. Repertoire, Genealogy and Genomic Organization of Cruzipain and Homologous Genes in Trypanosoma cruzi, T. cruzi-Like and Other Trypanosome Species. Lima L, Ortiz PA, da Silva FM, Alves JM, Serrano MG, Cortez AP, Alfieri SC, Buck GA, Teixeira MM. Source Departamento de Parasitologia, ICB, Universidade de São Paulo, São Paulo, São Paulo, Brasil. Abstract Trypanosoma cruzi, the agent of Chagas disease, is a complex of genetically diverse isolates highly phylogenetically related to T. cruzi-like species, Trypanosoma cruzi marinkellei and Trypanosoma dionisii, all sharing morphology of blood and culture forms and development within cells. However, they differ in hosts, vectors and pathogenicity: T. cruzi is a human pathogen infective to virtually all mammals whilst the other two species are non-pathogenic and bat restricted. Previous studies suggest that variations in expression levels and genetic diversity of cruzipain, the major isoform of cathepsin L-like (CATL) enzymes of T. cruzi, correlate with levels of cellular invasion, differentiation, virulence and pathogenicity of distinct strains. In this study, we compared 80 sequences of genes encoding cruzipain from 25 T. cruzi isolates representative of all discrete typing units (DTUs TcI-TcVI) and the new genotype Tcbat and 10 sequences of homologous genes from other species. The catalytic domain repertoires diverged according to DTUs and trypanosome species. Relatively homogeneous sequences are found within and among isolates of the same DTU except TcV and TcVI, which displayed sequences unique or identical to those of TcII and TcIII, supporting their origin from the hybridization between these two DTUs. In network genealogies, sequences from T. cruzi clustered tightly together and closer to T. c. marinkellei than to T. dionisii and largely differed from homologues of T. rangeli and T. b. brucei. Here, analysis of isolates representative of the overall biological and genetic diversity of T. cruzi and closest T. cruzi-like species evidenced DTU- and species-specific polymorphisms corroborating phylogenetic relationships inferred with other genes. Comparison of both phylogenetically close and distant trypanosomes is valuable to understand host-parasite interactions, virulence and pathogenicity. Our findings corroborate cruzipain as valuable target for drugs, vaccine, diagnostic and genotyping approaches.
	PMID: 22685565 [PubMed - in process]

2.	J Trop Med. 2012;2012:601242. Epub 2012 May 20. Leishmaniasis and climate change-case study: Argentina. Salomón OD, Quintana MG, Mastrángelo AV, Fernández MS. Source Instituto Nacional de Medicina Tropical, Neuquén y Jujuy, Puerto Iguazú, Consejo Nacional de Investigaciones Científicas y Técnicas CONICET CP3370, Argentina. Abstract Vector-borne diseases closely associated with the environment, such as leishmaniases, have been a usual argument about the deleterious impact of climate change on public health. From the biological point of view interaction of different variables has different and even conflicting effects on the survival of vectors and the probability transmission of pathogens. The results on ecoepidemiology of leishmaniasis in Argentina related to climate variables at different scales of space and time are presented. These studies showed that the changes in transmission due to change or increase in frequency and intensity of climatic instability were expressed through changes in the probability of vector-human reservoir effective contacts. These changes of contact in turn are modulated by both direct effects on the biology and ecology of the organisms involved, as by perceptions and changes in the behavior of the human communities at risk. Therefore, from the perspective of public health and state policy, and taking into account the current nonlinear increased velocity of climate change, we concluded that discussing the uncertainties of large-scale models will have lower impact than to develop-validate mitigation strategies to be operative at local level, and compatibles with sustainable development, conservation biodiversity, and respect for cultural diversity.
	PMID: 22685477 [PubMed - in process]

3.	J Immunol. 2012 Jun 8. [Epub ahead of print] Leishmania donovani Exploits Host Deubiquitinating Enzyme A20, a Negative Regulator of TLR Signaling, To Subvert Host Immune Response. Srivastav S, Kar S, Chande AG, Mukhopadhyaya R, Das PK. Source Infectious Diseases and Immunology Division, Molecular Cell Biology Laboratory, Indian Institute of Chemical Biology, Kolkata 700032, India. Abstract TLRs, which form an interface between mammalian host and microbe, play a key role in pathogen recognition and initiation of proinflammatory response thus stimulating antimicrobial activity and host survival. However, certain intracellular pathogens such as Leishmania can successfully manipulate the TLR signaling, thus hijacking the defensive strategies of the host. Despite the presence of lipophosphoglycan, a TLR2 ligand capable of eliciting host-defensive cytokine response, on the surface of Leishmania, the strategies adopted by the parasite to silence the TLR2-mediated proinflammatory response is not understood. In this study, we showed that Leishmania donovani modulates the TLR2-mediated pathway in macrophages through inhibition of the IKK-NF-κB cascade and suppression of IL-12 and TNF-α production. This may be due to impairment of the association of TRAF6 with the TAK-TAB complex, thus inhibiting the recruitment of TRAF6 in TLR2 signaling. L. donovani infection drastically reduced Lys 63-linked ubiquitination of TRAF6, and the deubiquitinating enzyme A20 was found to be significantly upregulated in infected macrophages. Small interfering RNA-mediated silencing of A20 restored the Lys 63-linked ubiquitination of TRAF6 as well as IL-12 and TNF-α levels with a concomitant decrease in IL-10 and TGF-β synthesis in infected macrophages. Knockdown of A20 led to lower parasite survival within macrophages. Moreover, in vivo silencing of A20 by short hairpin RNA in BALB/c mice led to increased NF-κB DNA binding and host-protective proinflammatory cytokine response resulting in effective parasite clearance. These results suggest that L. donovani might exploit host A20 to inhibit the TLR2-mediated proinflammatory gene expression, thus escaping the immune responses of the host.
	PMID: 22685311 [PubMed - as supplied by publisher]

4.	Nucleic Acids Res. 2012 Jun 7. [Epub ahead of print] Identification of the regulatory elements controlling the transmission stage-specific gene expression of PAD1 in Trypanosoma brucei. Macgregor P, Matthews KR. Source Centre for Immunity, Infection and Evolution, Institute for Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, King's buildings, West Mains Road, Edinburgh, EH9 3JTU, UK. Abstract Trypanosomatid parasites provide an extreme model for the posttranscriptional control of eukaryotic gene expression. However, most analysis of their differential gene regulation has focussed on comparisons between life-cycle stages that exist in the blood of mammalian hosts and tsetse flies, the parasite's vector. These environments differ acutely in their temperature, and nutritional, metabolic and molecular composition. In the bloodstream, however, a more exquisitely regulated developmental step occurs: the production of transmissible stumpy forms from proliferative slender forms. This transition occurs in the relatively homogenous bloodstream environment, with stumpy-specific gene expression being repressed until accumulation of a proposed parasite-derived signal, stumpy induction factor. Here, we have dissected the regulatory signals that repress the expression of the stumpy-specific surface transporter PAD1 in slender forms. Using transgenic parasites capable of stumpy formation we show that PAD1-repression is mediated by its 3'-untranslated region. Dissection of this region in monomorphic slender forms and pleomorphic slender and stumpy forms has revealed that two regulatory regions co-operate to repress PAD1 expression, this being alleviated on exposure to SIF in pleomorphs or cAMP analogues that act as stumpy induction factor mimics in monomorphs. These studies identify elements that regulate trypanosome gene expression during development in their mammalian host.
	PMID: 22684509 [PubMed - as supplied by publisher]

5.	J Insect Physiol. 2012 Jun 7. [Epub ahead of print] Relationship between digestive enzymes and food habit of Lutzomyia longipalpis (Diptera: Psychodidae) larvae: characterization of carbohydrases and digestion of microorganisms. Moraes CS, Lucena SA, Moreira BH, Brazil RP, Gontijo NF, Genta FA. Source Oswaldo Cruz Institute, FIOCRUZ, Rio de Janeiro, Brazil. Abstract The sandfly Lutzomyia longipalpis (Lutz and Neiva, 1912) is the main vector of American Visceral Leishmaniasis. In spite of its medical importance and several studies concerning adult digestive physiology, biochemistry and molecular biology, very few studies have been carried out to elucidate the digestion in sandfly larvae. Even the breeding sites and food sources of these animals in the field are largely uncharacterized. In this paper, we describe and characterize several carbohydrases from the gut of L. longipalpis larvae, and show that they are probably not acquired from food. The enzyme profile of this insect is consistent with the digestion of fungal and bacterial cells, which were proved to be ingested by larvae under laboratory conditions. In this respect, sandfly larvae might have a detritivore habit in nature, being able to exploit microorganisms usually encountered in the detritus as a food source. Copyright © 2012 Elsevier Ltd. All rights reserved.
	PMID: 22684112 [PubMed - as supplied by publisher]

6.	Biochim Biophys Acta. 2012 Jun 7. [Epub ahead of print] A leishmaniasis study: Structure-based screening and molecular dynamics mechanistic analysis for discovering potent inhibitors of spermidine synthase. Grover A, Katiyar SP, Singh SK, Dubey VK, Sundar D. Source Department of Biochemical Engineering and Biotechnology, Indian Institute of Technology (IIT) Delhi, Hauz Khas, New Delhi 110016, India. Abstract Protozoa Leishmania donovani (Ld) is the main cause of the endemic disease leishmaniasis. Spermidine synthase (SS), an important enzyme in the synthetic pathway of polyamines in Ld, is an essential element for the survival of this protozoan. Targeting SS may provide an important aid for the development of drugs against Ld. However, absence of tertiary structure of spermidine synthase of Leishmania donovani (LSS) limits the possibilities of structure based drug designing. Presence of the same enzyme in the host itself further challenges the drug development process. We modelled the tertiary structure of LSS using homology modelling approach making use of homologous X-ray crystallographic structure of spermidine synthase of Trypanosoma cruzi (TSS) (2.5Å resolution). The modelled structure was stabilized using Molecular Dynamics simulations. Based on active site structural differences between LSS and human spermidine synthase (HSS), we screened a large dataset of compounds against modelled protein using Glide virtual screen docking and selected two best inhibitors based on their docking scores (-10.04 and -13.11 respectively) with LSS and having least/no binding with the human enzyme. Finally Molecular Dynamics simulations were used to assess the dynamic stability of the ligand bound structures and to elaborate on the binding modes. This article is part of a Special Issue entitled: Computational Methods for Protein Interaction and Structural Prediction. Copyright © 2012. Published by Elsevier B.V.
	PMID: 22684087 [PubMed - as supplied by publisher]

7.	Microbes Infect. 2012 Jun 6. [Epub ahead of print] Leishmania virulence factors: Focus on the metalloprotease GP63. Olivier M, Atayde VD, Isnard A, Hassani K, Shio MT. Source Department of Medicine, Microbiology and Immunology, the Research Institute of the McGill University Health Centre, Faculty of Medicine, McGill University, Montréal, Qc, Canada. Abstract Parasites of Leishmania genus have developed elegant strategies permitting them to evade the innate immune response upon their initial interaction with macrophages. Their capacity to dodge the induction of macrophages microbicidal functions was found to correlate with the alteration of several signalling pathways regulating those latter. In this review, the role of the Leishmania GP63 as a critical virulence factor influencing macrophage physiology will be discussed. Copyright © 2012. Published by Elsevier Masson SAS.
	PMID: 22683718 [PubMed - as supplied by publisher]

8.	J Pediatr. 2012 Jun 8. [Epub ahead of print] Leishmaniasis: A Reminder in the Face of Forgotten Travel. Terhorst D, Blume-Peytavi U, Schönian G, Schewe C, Haas N, Burbach GJ. Source Department of Dermatology and Allergy, Charité-Universitätsmedizin Berlin, Berlin, Germany; Centre D'Immunologie de Marseille-Luminy, Parc Scientifique & Technologique de Luminy, Marseille, France.
	PMID: 22683034 [PubMed - as supplied by publisher]

9.	Clin Dermatol. 2012 Jul;30(4):420-4. Lobomycosis. Talhari S, Talhari C. Source Faculty of Medicine, Nilton Liins University, Av. Professor Nilton Lins, 3259. Parque das Laranjeiras, Manaus, Amazonas, Brazil. Abstract Lobomycosis is a rare chronic fungal infection of the subcutaneous tissue found in South America, mainly in Brazil. It is caused by Lacazia loboi. Its clinical manifestations are dermal nodules, either lenticular or in plaques, and keloidlike lesions that can resemble nodular leprosy or leishmaniasis, other subcutaneous mycoses (sporotrychosis, chromomycosis, paracoccidioidomycosis), keloids, and malignant tumors. Diagnosis is made by the histopathological findings of the fungus. For treatment, surgical removal of the lesions, followed by itraconazole and clofazimine for disseminated lesions, has been used with variable results. Copyright © 2012. Published by Elsevier Inc.
	PMID: 22682191 [PubMed - in process]

10.	J Nat Prod. 2012 Jun 8. [Epub ahead of print] Albopunctatone, an Antiplasmodial Anthrone-Anthraquinone from the Australian Ascidian Didemnum albopunctatum. Carroll AR, Nash BD, Duffy S, Avery VM. Source School of Environment, Griffith University , Gold Coast, QLD 4222, Australia. Abstract Chemical investigation of a MeOH extract of the Great Barrier Reef ascidian Didemnum albopunctatum has led to the isolation and identification of a new anthrone-anthraquinone, albopunctatone (1), together with the known 1,8-dihydroxy-9,10-anthraquinone (2). The structure of 1 was established from interpretation of 1D and 2D NMR spectroscopic and mass spectrometric data. The compounds were screened for antiplasmodial activity against chloroquine-resistant and -sensitive strains of the malaria parasite, Plasmodium falciparum. Albopunctatone (1) was moderately active against both strains (IC(50) 5.3 and 4.4 ± 0.5 μM, respectively), while 2 was inactive at doses up to 40 μM. Both compounds were also inactive up to 40 μM when tested against a variety of cancerous and normal human cell lines and the kinetoplastid Trypanosoma brucei brucei, indicating selectivity for the malaria parasite, P. falciparum.
	PMID: 22680914 [PubMed - as supplied by publisher]