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Sent on Friday, 2010 May 21Search 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 Clin Lab Anal. 2010 00;24(3):187-194.Application of monoclonal antibodies to measure metabolism of an anti-trypanosomal compound in vitro and in vivo.Goldsmith RB, Gray DR, Yan Z, Generaux CN, Tidwell RR, Reisner HM.Department of Pathology and Laboratory Medicine, School of Medicine, University of North Carolina, Chapel Hill, North Carolina. AbstractHuman African trypanosomiasis (HAT), also called African sleeping sickness, is a neglected tropical parasitic disease indigenous to sub-Saharan Africa. Diamidine compounds, including pentamidine and CPD-0801, are potent anti-trypanosomal molecules. The latter is a potential drug in the development at the UNC based Consortium for Parasitic Drug Development. An orally bioavailable prodrug of CPD-0801, DB868, is metabolized primarily in the liver to the active form. A monoclonal antibody developed against a pentamidine derivative has shown significant reactivity with CPD-0801 (EC(50) 65.1 nM), but not with the prodrug (EC(50)>18,000 nM). An inhibitory enzyme-linked immunosorbent assay (IELISA) has been used to quantitatively monitor prodrug metabolism by detecting the production of the active compound over time in a sandwich culture rat hepatocyte system and in rats. These results were compared with the results of the standard LC/MS/MS assay. Spearman coefficients of 0.96 and 0.933 (in vitro and in vivo, respectively) indicate a high correlation between these two measurement methods. This novel IELISA provides a facile, inexpensive, and accurate method for drug detection that may aide in elucidating the mechanisms of action and toxicity of existing and future diamidine compounds. J. Clin. Lab. Anal. 24:187-194, 2010. (c) 2010 Wiley-Liss, Inc. |
| PMID: 20486201 [PubMed - as supplied by publisher] | |
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| 2. | Salud Publica Mex. 2010 Apr;52(2):165-9.[Reaction of Leishmania (Leishmania) mexicana antigens by sera of patients with cutaneous leishmaniasis from Sinaloa, Mexico.][Article in Spanish] Salazar-Mejía PG, Tejeda-Aguirre CR, López-Moreno HS.Laboratorio de Biomedicina, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Sinaloa, Sinaloa, México. AbstractOBJECTIVE: To detect Leishmania mexicana antigens reacting with sera of patients with cutaneous leishmaniasis (CL). MATERIAL AND METHODS: A crude extract of L. mexicana was used as antigen for 2-D Western blot using sera from 5 patients with CL and controls from Sinaloa, Mexico during 2008. RESULTS: Five antigens were detected in the five infected patients analyzed; their molecular weights and isoelectric points were: 26 kDa (pI 7.8), 27 kDa (pI 8.1), 28 kDa (pI 8.6), 29 kDa (pI 8.5) and 31 kDa (pI 9.0). CONCLUSION: New potentially immunodominant L. mexicana antigens were detected, suggesting that this parasite could be the species responsible for human infection in Sinaloa. |
| PMID: 20485874 [PubMed - in process] | |
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| 3. | J Immunol. 2010 May 12. [Epub ahead of print]Type I IFN Receptor Regulates Neutrophil Functions and Innate Immunity to Le ishmania Parasites.Xin L, Vargas-Inchaustegui DA, Raimer SS, Kelly BC, Hu J, Zhu L, Sun J, Soong L.Department of Microbiology and Immunology. AbstractType I IFNs exert diverse effector and regulatory functions in host immunity to viral and nonviral infections; however, the role of endogenous type I IFNs in leishmaniasis is unclear. We found that type I IFNR-deficient (IFNAR(-/-)) mice developed attenuated lesions and reduced Ag-specific immune responses following infection with Leishmania amazonensis parasites. The marked reduction in tissue parasites, even at 3 d in IFNAR(-/-) mice, seemed to be indicative of an enhanced innate immunity. Further mechanistic analyses indicated distinct roles for neutrophils in parasite clearance; IFNAR(-/-) mice displayed a rapid and sustained infiltration of neutrophils, but a limited recruitment of CD11b(+)Ly-6C(+) inflammatory monocytes, into inflamed tissues; interactions between IFNAR(-/-), but not wild-type (WT) or STAT1(-/-), neutrophils and macrophages greatly enhanced parasite killing in vitro; and infected IFNAR(-/-) neutrophils efficiently released granular enzymes and had elevated rates of cell apoptosis. Furthermore, although coinjection of parasites with WT neutrophils or adoptive transfer of WT neutrophils into IFNAR(-/-) recipients significantly enhanced infection, the coinjection of parasites with IFNAR(-/-) neutrophils greatly reduced parasite survival in WT recipients. Our findings reveal an important role for type I IFNs in regulating neutrophil/monocyte recruitment, neutrophil turnover, and Leishmania infection and provide new insight into innate immunity to protozoan parasites. |
| PMID: 20483775 [PubMed - as supplied by publisher] | |
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| 4. | Trends Parasitol. 2010 May 17. [Epub ahead of print]Glycolipids are potential targets for protozoan parasite diseases.Debierre-Grockiego F.UMR Université-INRA 0483, UFR Sciences Pharmaceutiques, Immunologie Parasitaire, Vaccinologie et Biothérapies anti-infectieuses, 31 Avenue Monge, F-37200 Tours, France. AbstractInduction of sterilizing immunity by vaccination is extremely difficult because of the evasion mechanisms developed by parasites, and identification of new targets for therapy is therefore important. Glycosylphosphatidylinositols (GPIs) of parasites are glycolipids that participate in pathogenicity of parasitic diseases. Studies of Plasmodium falciparum and Trypanosoma brucei indicate that GPIs are good candidates for developing vaccines against malaria and sleeping sickness, respectively. By contrast, fatty acids isolated from P. falciparum and Toxoplasma gondii can inhibit the production of inflammatory cytokines induced by the GPIs in macrophages. GPIs are considered to be toxins that, if present in large amounts, induce irreversible damages to the host, and treatment with fatty acids could reduce this effect. Copyright © 2010 Elsevier Ltd. All rights reserved. |
| PMID: 20483663 [PubMed - as supplied by publisher] | |
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| 5. | DNA Cell Biol. 2010 May;29(5):213.Highlights from the May 2010 issue of DNA and Cell Biology: unusual systems and techniques.Handelsman J. |
| PMID: 20465427 [PubMed - indexed for MEDLINE] | |
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| 6. | Nature. 2010 Apr 1;464(7289):689-90.Drug discovery: Fat-free proteins kill parasites.Cross GA.Comment on: |
| PMID: 20360728 [PubMed - indexed for MEDLINE] | |
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| 7. | PLoS Negl Trop Dis. 2010 Mar 2;4(3):e613.Role of GP82 in the selective binding to gastric mucin during oral infection with Trypanosoma cruzi.Staquicini DI, Martins RM, Macedo S, Sasso GR, Atayde VD, Juliano MA, Yoshida N.Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, São Paulo, Brasil. AbstractOral infection by Trypanosoma cruzi has been the primary cause of recent outbreaks of acute Chagas' diseases. This route of infection may involve selective binding of the metacyclic trypomastigote surface molecule gp82 to gastric mucin as a first step towards invasion of the gastric mucosal epithelium and subsequent systemic infection. Here we addressed that question by performing in vitro and in vivo experiments. A recombinant protein containing the complete gp82 sequence (J18), a construct lacking the gp82 central domain (J18*), and 20-mer synthetic peptides based on the gp82 central domain, were used for gastric mucin binding and HeLa cell invasion assays, or for in vivo experiments. Metacyclic trypomastigotes and J18 bound to gastric mucin whereas J18* failed to bind. Parasite or J18 binding to submaxillary mucin was negligible. HeLa cell invasion by metacyclic forms was not affected by gastric mucin but was inhibited in the presence of submaxillary mucin. Of peptides tested for inhibition of J18 binding to gastric mucin, the inhibitory peptide p7 markedly reduced parasite invasion of HeLa cells in the presence of gastric mucin. Peptide p7*, with the same composition as p7 but with a scrambled sequence, had no effect. Mice fed with peptide p7 before oral infection with metacyclic forms developed lower parasitemias than mice fed with peptide p7*. Our results indicate that selective binding of gp82 to gastric mucin may direct T. cruzi metacyclic trypomastigotes to stomach mucosal epithelium in oral infection. |
| PMID: 20209152 [PubMed - indexed for MEDLINE] | |
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| 8. | Biochemistry. 2010 Apr 6;49(13):2778-85.A temperature-induced narrow DNA curvature range sustains the maximum activity of a bacterial promoter in vitro.Prosseda G, Mazzola A, Di Martino ML, Tielker D, Micheli G, Colonna B.Istituto Pasteur Fondazione Cenci Bolognetti, Dip. Biologia Cellulare e dello Sviluppo, Sapienza Univ. Roma, via dei Sardi 70, 00185 Roma, Italy. AbstractAmong the molecular strategies bacteria have set up to quickly match their transcriptional program to new environments, changes in sequence-mediated DNA curvature play a crucial role. Bacterial promoters, especially those of mesophilic bacteria, are in general preceded by a curved region. The marked thermosensitivity of curved DNA stretches allows bacteria to rapidly sense outer temperature variations and affects transcription by favoring the binding of activators or repressors. Curved DNA is also able to influence the transcriptional activity of a bacterial promoter directly, without the involvement of trans-acting regulators. This study attempts to quantitatively analyze the role of DNA curvature in thermoregulated gene expression using a real-time in vitro transcription model system based on a specific fluorescence molecular beacon. By analyzing the temperature-dependent expression of a reporter gene in a construct carrying a progressively decreasing bent sequence upstream from the promoter, we show that with a decrease in temperature a narrow curvature range accounts for a significant enhancement of promoter activity. This strengthens the view that DNA curvature-mediated regulation of gene expression is likely a strategy offering fine-tuning control possibilities and that, considering the widespread presence of curved sequences upstream from bacterial promoters, it may represent one of the most primitive forms of gene regulation. |
| PMID: 20170130 [PubMed - indexed for MEDLINE] | |
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| 9. | Parasitol Res. 2010 Mar;106(4):985-9. Epub 2010 Feb 6.Trypanocidal activity and acute toxicity assessment of triterpene acids.Ferreira Dda S, Esperandim VR, Toldo MP, Saraiva J, Cunha WR, de Albuquerque S.Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brazil. danisf@fcfrp.usp.br AbstractThe present study evaluates the in vitro and in vivo trypanocidal activity of ursolic acid and oleanolic acid against the Bolivia strain of Trypanosoma cruzi. Their acute toxicity is also assessed on the basis of median lethal dose (DL50) determination and quantification of biochemical parameters. Ursolic acid is the most active compound in vitro, furnishing IC50 of 25.5 microM and displaying 77% of trypomastigote lysis at a concentration of 128 microM. In agreement with in vitro assays, the results obtained for the in vivo assay reveals that ursolic acid (at a dose of 20 mg/Kg/day) provides the most significant reduction in the number of parasites at the parasitemic peak. Results concerning the LD50 assay and the biochemical parameters evaluated in the present study demonstrate that these substances can be safely used on an experimental basis. |
| PMID: 20140451 [PubMed - indexed for MEDLINE] | |
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| 10. | PLoS One. 2010 Jan 20;5(1):e7764.Dynasore, a dynamin inhibitor, inhibits Trypanosoma cruzi entry into peritoneal macrophages.Barrias ES, Reignault LC, De Souza W, Carvalho TM.Laboratório de Ultraestrutura Celular Hertha Meyer, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, CCS-Bloco G, Ilha do Fundão, Rio de Janeiro, Brasil. AbstractBACKGROUND: Trypanosoma cruzi is an intracellular parasite that, like some other intracellular pathogens, targets specific proteins of the host cell vesicular transport machinery, leading to a modulation of host cell processes that results in the generation of unique phagosomes. In mammalian cells, several molecules have been identified that selectively regulate the formation of endocytic transport vesicles and the fusion of such vesicles with appropriate acceptor membranes. Among these, the GTPase dynamin plays an important role in clathrin-mediated endocytosis, and it was recently found that dynamin can participate in a phagocytic process. METHODOLOGY/PRINCIPAL FINDINGS: We used a compound called dynasore that has the ability to block the GTPase activity of dynamin. Dynasore acts as a potent inhibitor of endocytic pathways by blocking coated vesicle formation within seconds of its addition. Here, we investigated whether dynamin is involved in the entry process of T. cruzi in phagocytic and non-phagocytic cells by using dynasore. In this aim, peritoneal macrophages and LLC-MK2 cells were treated with increasing concentrations of dynasore before interaction with trypomastigotes, amastigotes or epimastigotes. We observed that, in both cell lines, the parasite internalization was drastically diminished (by greater than 90% in LLC-MK2 cells and 70% in peritoneal macrophages) when we used 100 microM dynasore. The T. cruzi adhesion index, however, was unaffected in either cell line. Analyzing these interactions by scanning electron microscopy and comparing peritoneal macrophages to LLC-MK2 cells revealed differences in the stage at which cell entry was blocked. In LLC-MK2 cells, this blockade is observed earlier than it is in peritoneal macrophages. In LLC-MK2 cells, the parasites were only associated with cellular microvilli, whereas in peritoneal macrophages, trypomastigotes were not completely engulfed by a host cell plasma membrane. CONCLUSIONS/SIGNIFICANCE: Taken together our results demonstrate that dynamin is an essential molecule necessary for cell invasion and specifically parasitophorous vacuole formation by host cells during interaction with Trypanosoma cruzi. |
| PMID: 20098746 [PubMed - indexed for MEDLINE] | |
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