What's new for 'Trypanosomatids' in PubMed

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Sent on Wednesday, 2010 Jun 30
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 - 8 of 8

1.	PLoS One. 2010 Jun 23;5(6):e11271. Ascorbate Peroxidase from Leishmania major Controls the Virulence of Infective Stage of Promastigotes by Regulating Oxidative Stress. Pal S, Dolai S, Yadav RK, Adak S. Division of Structural Biology & Bio-Informatics, Indian Institute of Chemical Biology, Kolkata, West Bengal, India. Abstract BACKGROUND: Peroxidase represents a heterogeneous group of distinct enzyme family that plays extremely diverse biological functions. Ascorbate peroxidase from Leishmania major (LmAPX) has been shown to be central to the redox defense system of Leishmania. To investigate further its exact physiological role in Leishmania, we attempted to create LmAPX -knockout mutants by gene replacement in L. major strains. METHODOLOGY/PRINCIPAL FINDINGS: The null mutant cell culture contains a higher percentage of metacyclic and apoptotic cells compared to both wild type and LmAPX overexpressing cells. Flowcytometric analysis reveals the presence of a higher concentration of intracellular H(2)O(2), indicative of increased oxidative stress in parasites lacking LmAPX. IC(50) value for exogenously added H(2)O(2) shows that deletion of LmAPX in L. major renders the cell more susceptible to H(2)O(2). Real time PCR studies demonstrate an elevated mRNA level of non-selenium glutathione peroxidase in LmAPX null mutant cell line, suggesting that these enzymes were induced to compensate the LmAPX enzyme. The null mutant cells exhibit hypervirulence after infection with macrophages as well as inoculation into BALB/c mice; in contrast, overexpressing cells show avirulence. CONCLUSIONS/SIGNIFICANCE: Collectively, these data provide strong evidence that LmAPX is an important factor for controlling parasite differentiation and survival within macrophages.
	PMID: 20585663 [PubMed - in process]
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2.	PLoS Pathog. 2010 Jun 17;6(6):e1000899. Modulation of the arginase pathway in the context of microbial pathogenesis: a metabolic enzyme moonlighting as an immune modulator. Das P, Lahiri A, Lahiri A, Chakravortty D. Center for Infectious Disease Research and Biosafety Laboratories, Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India. Abstract Arginine is a crucial amino acid that serves to modulate the cellular immune response during infection. Arginine is also a common substrate for both inducible nitric oxide synthase (iNOS) and arginase. The generation of nitric oxide from arginine is responsible for efficient immune response and cytotoxicity of host cells to kill the invading pathogens. On the other hand, the conversion of arginine to ornithine and urea via the arginase pathway can support the growth of bacterial and parasitic pathogens. The competition between iNOS and arginase for arginine can thus contribute to the outcome of several parasitic and bacterial infections. There are two isoforms of vertebrate arginase, both of which catalyze the conversion of arginine to ornithine and urea, but they differ with regard to tissue distribution and subcellular localization. In the case of infection with Mycobacterium, Leishmania, Trypanosoma, Helicobacter, Schistosoma, and Salmonella spp., arginase isoforms have been shown to modulate the pathology of infection by various means. Despite the existence of a considerable body of evidence about mammalian arginine metabolism and its role in immunology, the critical choice to divert the host arginine pool by pathogenic organisms as a survival strategy is still a mystery in infection biology.
	PMID: 20585552 [PubMed - in process]
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3.	Photodermatol Photoimmunol Photomed. 2010 Jun;26(3):118-32. Photodynamic therapy in dermatology: state-of-the-art. Babilas P, Schreml S, Landthaler M, Szeimies RM. Department of Dermatology, University Hospital Regensburg, Regensburg, Germany. Abstract Photodynamic therapy (PDT) has become an established treatment modality for dermatooncologic conditions like actinic keratosis, Bowen's disease, in situ squamous cell carcinoma and superficial basal cell carcinoma. There is also great promise of PDT for many non-neoplastic dermatological diseases like localized scleroderma, acne vulgaris, granuloma anulare and leishmaniasis. Aesthetic indications like photo-aged skin or sebaceous gland hyperplasia complete the range of applications. Major advantages of PDT are the low level of invasiveness and the excellent cosmetic results. Here, we review the principal mechanism of action, the current developments in the field of photosensitizers and light sources, practical aspects of topical PDT and therapeutical applications in oncologic as well as non-oncologic indications.
	PMID: 20584250 [PubMed - in process]
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4.	J Infect Dis. 2010 Jun 28. [Epub ahead of print] T-bet, GATA-3, and Foxp3 Expression and Th1/Th2 Cytokine Production in the Clinical Outcome of Human Infection with Leishmania (Viannia) Species. Díaz YR, Rojas R, Valderrama L, Saravia NG. Centro Internacional de Entrenamiento e Investigaciones Médicas (CIDEIM), Cali, Colombia. Abstract Background. T cell differentiation determines susceptibility and resistance to experimental cutaneous leishmaniasis, yet mixed T1/Th2 responses characterize the clinical spectrum of human infection with Leishmania (Viannia) species. Materials and Methods. To discern the interrelationship of T cell differentiation and outcome of human infection, we examined factors that regulate T cell differentiation and Th1/Th2 cytokine responses in asymptomatic infection, active and historical chronic and recurrent cutaneous leishmaniasis. T-bet, GATA-3, Foxp3, and cytokine gene expression were quantified by real-time polymerase chain reaction and correlated with interleukin 2, interferon gamma, tumor necrosis factor alpha, interleukin 4, interleukin 13, and interleukin 10 secretion during in vitro response to live Leishmania panamensis. Results. Higher GATA-3 expression than T-bet expression occurred throughout the 15 days of coculture with promastigotes; however, neither transcription nor secretion of interleukin 4 was detected. A sustained inverse correlation between GATA-3 expression and secretion of proinflammatory cytokines interferon gamma and tumor necrosis factor alpha was observed in asymptomatic infection. In contrast, higher T-bet expression and a higher ratio of T-bet to GATA-3 characterized active recurrent disease. Down-regulation of T-bet and GATA-3 expression and increased interleukin 2 secretion, compared with control subjects, was directly correlated with Foxp3 expression and interleukin 13 secretion in chronic disease. Conclusions. Regulation of the inflammatory response rather than biased Th1/Th2 response distinguished asymptomatic and recalcitrant outcomes of infection with Leishmnania viannia species.
	PMID: 20583921 [PubMed - as supplied by publisher]
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5.	J Proteome Res. 2010 Jun 28. [Epub ahead of print] Analysis of stage-specific expression of basic proteins in Leishmania infantum. Brotherton MC, Racine G, Foucher A, Drummelsmith J, Papadopoulou B, Ouellette M. Abstract Prior analyses of the proteome of the protozoan parasite Leishmania have underrepresented basic proteins. Here, we applied protein fractionation by isoelectric point (pI) using free-flow electrophoresis (FFE) to study stage-specific expression of basic proteins in this pathogen. Overall, we resolved 2469 protein spots in both the flagellated promastigote and the non-motile amastigote forms in the basic range by two-dimensional gel electrophoresis (2DE). Highly basic proteins were enriched by FFE fractionation, allowing many to be identified and characterized for the first time by proteomics analysis. Among proteins upregulated in the promastigote stage, we found glycolytic enzymes and flagellar proteins. Proteins upregulated in the amastigote stage included enzymes involved in gluconeogenesis and fatty acid beta-oxidation. In both life stages, many proteins were found in multiple spots or as proteolytic fragments, suggesting that extensive post-translational modification and processing occur. Interestingly, evidence was obtained suggesting that some of these processes may be stage-specific.
	PMID: 20583757 [PubMed - as supplied by publisher]
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6.	Parasite Immunol. 2010 Apr;32(4):245-51. Enhanced protection by melatonin and meloxicam combination in experimental infection by Trypanosoma cruzi. Olivei ra LG, Kuehn CC, Santos CD, Toldo MP, do Prado JC Jr. Laboratório de Parasitologia, Departamento de Análises Clínicas, Toxicológicas e Bromatológicas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto FCFRP-USP, Universidade de São Paulo, Ribeirão Preto, SP, Brasil. Abstract The aim of this study was to evaluate a possible synergism between melatonin and meloxicam in up-regulating the immune response in male Wistar rats infected with Trypanosoma cruzi during immunosuppression phenomenon, which characterizes the acute phase of the Chagas' disease. Male Wistar rats were infected with the Y strain of T. cruzi. Experiments were performed on 7, 14 and 21 days post-infection. Several immunological parameters were evaluated including gamma-interferon (IFN-gamma), interleukin-2 (IL-2), nitric oxide (NO) and prostaglandin E(2) (PGE(2)). The combined treatment with melatonin and meloxicam significantly enhanced the release of IL-2 and INF-gamma into animals' serum, when compared with the infected control groups during the course of infection. Furthermore, the blockade of PGE(2) synthesis and the increased release of NO by macrophage cells from T. cruzi-infected animals contributed to regulate the production of Th1 subset cytokines significantly reducing the parasitaemia in animals treated with the combination of both substances. Therefore, our results suggest that the association of melatonin and meloxicam was more effective in protecting animals against the harmful actions of T. cruzi infection as compared with the treatments of meloxicam or melatonin alone.
	PMID: 20398224 [PubMed - indexed for MEDLINE]
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7.	Neth J Med. 2010 Mar;68(3):144-5. Tryps after adventurous trips. Claessen FA, Blaauw GJ, van der Vorst MJ, Ang CW, van Agtmael MA. Free Article
	PMID: 20308714 [PubMed - indexed for MEDLINE]
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8.	J Bioenerg Biomembr. 2010 Feb;42(1):69-78. Epub 2010 Feb 13. Mechanism of Trypanosoma cruzi death induced by Cratylia mollis seed le ctin. Fernandes MP, Inada NM, Chiaratti MR, Araújo FF, Meirelles FV, Correia MT, Coelho LC, Alves MJ, Gadelha FR, Vercesi AE. Departamento de Patologia Clínica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Campinas, Brazil. Abstract Incubation of T. cruzi epimastigotes with the lectin Cramoll 1,4 in Ca(2+) containing medium led to agglutination and inhibition of cell proliferation. The lectin (50 microg/ml) induced plasma membrane permeabilization followed by Ca(2+) influx and mitochondrial Ca(2+) accumulation, a result that resembles the classical effect of digitonin. Cramoll 1,4 stimulated (five-fold) mitochondrial reactive oxygen species (ROS) production, significantly decreased the electrical mitochondrial membrane potential (Delta Psi(m)) and impaired ADP phosphorylation. The rate of uncoupled respiration in epimastigotes was not affected by Cramoll 1,4 plus Ca(2+) treatment, but oligomycin-induced resting respiration was 65% higher in treated cells than in controls. Experiments using T. cruzi mitochondrial fractions showed that, in contrast to digitonin, the lectin significantly decreased Delta Psi(m) by a mechanism sensitive to EGTA. In agreement with the results showing plasma membrane permeabilization and impairment of oxidative phosphorylation by the lectin, fluorescence microscopy experiments using propidium iodide revealed that Cramoll 1,4 induced epimastigotes death by necrosis.
	PMID: 20155390 [PubMed - indexed for MEDLINE]
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