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Sent on Thursday, 2010 Sep 02Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | Zhongguo Ji Sheng Chong Xue Yu Ji Sheng Chong Bing Za Zhi. 2010 Jun 30;28(3):209, 213.[Liposomal amphotericin B cured two cases of visceral leishmaniasis tolerant to sodium antimony gluconate][Article in Chinese] Yuan QR. |
| PMID: 20806506 [PubMed - in process] | |
| 2. | Proc Natl Acad Sci U S A. 2010 Aug 30. [Epub ahead of print]Mechanism of Trypanosoma brucei gambiense (group 1) resistance to human trypanosome lytic factor.Kieft R, Capewell P, Turner CM, Veitch NJ, Macleod A, Hajduk S.Department of Biochemistry and Molecular Biology, University of Georgia, Athens, GA 30602. AbstractHuman innate immunity against most African trypanosomes, including Trypanosoma brucei brucei, is mediated by a minor subclass of toxic serum HDL, called trypanosome lytic factor-1 (TLF-1). This HDL contains two primate specific proteins, apolipoprotein L-1 and haptoglobin (Hp)-related protein, as well as apolipoprotein A-1. These assembled proteins provide a powerful defense against trypanosome infection. Trypanosoma brucei rhodesiense causes human African sleeping sickness because it has evolved an inhibitor of TLF-1, serum resistance-associated (SRA) protein. Trypanosoma brucei gambiense lacks the SRA gene, yet it infects humans. As transfection of T. b. gambiense (group 1) is not possible, we initially used in vitro-selected TLF-1-resistant T. b. brucei to examine SRA-independent mechanisms of TLF-1 resistance. Here we show that TLF-1 resistance in T. b. brucei is caused by reduced expression of the Hp/Hb receptor gene (TbbHpHbR). Importantly, T. b. gambiense (group 1) also showed a marked reduction in uptake of TLF-1 and a corresponding decrease in expression of T. b. gambiense Hp/Hb receptor (TbgHpHbR). Ectopic expression of TbbHpHbR in TLF-1-resistant T. b. brucei rescued TLF-1 uptake, demonstrating that decreased TbbHpHbR expression conferred TLF-1 resistance. Ectopic expression of TbgHpHbR in TLF-1-resistant T. b. brucei failed to rescue TLF-1 killing, suggesting that coding sequence changes altered Hp/Hb receptor binding affinity for TLF-1. We propose that the combination of coding sequence mutations and decreased expression of TbgHpHbR directly contribute to parasite evasion of human innate immunity and infectivity of group 1 T. b. gambiense. |
| PMID: 20805508 [PubMed - as supplied by publisher] | |
| 3. | Eur J Med Chem. 2010 Aug 12. [Epub ahead of print]Design and synthesis of bioactive adamantanaminoalcohols and adamantanamines.Zoidis G, Kolocouris N, Kelly JM, Prathalingam SR, Naesens L, De Clercq E.Faculty of Pharmacy, Department of Pharmaceutical Chemistry, University of Athens, Panepistimioupoli-Zografou, GR-15771 Athens, Greece. AbstractAdamantanamines 16, 18, 21, 24, 27, 28, 30, 32, 35, 36, 37, 40, 46 and 48 were synthesized and tested for anti-influenza A virus and trypanocidal activity. The stereoelectronic requirements for optimal antiviral and trypanocidal potency were investigated. The effect of introducing a hydroxyl group close to the amino group on this class of compounds was examined for the first time. Aminoalcohol 24 proved to be the most active of the compounds tested against influenza A virus, being 6-fold more active than amantadine, equipotent to rimantadine and 26-fold more potent than ribavirin. Aminoalcohols 36 and 37 were found to have considerable activity against bloodstream forms of the African trypanosome, Trypanosoma brucei, being almost 10 times more potent than rimantadine. |
| PMID: 20805012 [PubMed - as supplied by publisher] | |
| 4. | Vector Borne Zoonotic Dis. 2010 Aug 30. [Epub ahead of print]A Serological and Molecular Study of Leishmania infantum Infection in Cats from the Island of Ibiza (Spain).Sherry K, Miró G, Trotta M, Miranda C, Montoya A, Espinosa C, Ribas F, Furlanello T, Solano-Gallego L.1 Department of Pathology and Infectious Diseases, Royal Veterinary College, University of London , United Kingdom . AbstractAbstract The aim of this study was to evaluate the prevalence of Leishmania infantum infection within a feline population by serologic and molecular methods and to identify associated risk factors. One hundred five cats living outdoors were studied. Sera were tested for IgG antibodies against L. infantum, Toxoplasma gondii, and feline immunodeficiency virus (FIV) and for the detection of feline leukemia virus (FeLV) p27 antigen by enzyme-linked immunosorbent assay (ELISA). L. infantum real-time polymerase chain reaction (PCR) was performed on DNA extracted from blood. L. infantum and T. gondii seroprevalence rates were 13.2% and 55.2%, respectively. The prevalence of L. infantum by PCR was 8.7%. The total rate of L. infantum infection derived from seroreactivity and/or positive PCR was 15.4%. Serology and PCR results were positively associated, and moderate agreement (kappa = 0.489) was found between Leishmania ELISA and PCR. No statistical association was found between positive Leishmania PCR results and gender, clinical status, or T. gondii seropositivity. Six of the 105 cats (5.7%) displayed clinical signs compatible with feline cutaneous leishmaniosis, and 4 out of these 6 cats (66.7%) were found to have Leishmania infection by means of serology and/or PCR. Leishmania seropositivity was associated with clinical signs of feline cutaneous leishmaniosis (p = 0.029). The prevalence of FeLV p27 antigen was 16.2% (17/105) and of FIV antibody was 20.9% (22/105), with coinfection found in 9.5% (10/105) of the cats. Leishmania ELISA seroreactivity and positive PCR results were statistically associated with FeLV infection and with coinfection of both retroviruses but not with a positive FIV status. The high seroprevalence and molecular rates of Leishmania infection observed indicate that cats are frequently infected with L. infantum, and the association with FeLV suggests a potential role for this retrovirus in feline Leishmania infection in endemic areas. |
| PMID: 20804432 [PubMed - as supplied by publisher] | |
| 5. | PLoS One. 2010 Jun 30;5(6):e11407.Structural changes of the paraflagellar rod during flagellar beating in Trypanosoma cruzi.Rocha GM, Teixeira DE, Miranda K, Weissmüller G, Bisch PM, de Souza W.Laboratório de Ultraestrutura Celular Hertha Meyer, Universidade Federal do Rio de Janeiro, Cidade Universitária, Ilha do Fundão, Rio de Janeiro, Brazil. AbstractBACKGROUND: Trypanosoma cruzi, the agent of Chagas disease, is a protozoan member of the Kinetoplastidae family characterized for the presence of specific and unique structures that are involved in different cell activities. One of them is the paraflagellar rod (PFR), a complex array of filaments connected to the flagellar axoneme. Although the function played by the PFR is not well established, it has been shown that silencing of the synthesis of its major proteins by either knockout of RNAi impairs and/or modifies the flagellar motility. METHODOLOGY/PRINCIPAL FINDINGS: Here, we present results obtained by atomic force microscopy (AFM) and transmission electron microscopy (TEM) of replicas of quick-frozen, freeze-fractured, deep-etched and rotary-replicated cells to obtain detailed information of the PFR structures in regions of the flagellum in straight and in bent state. The images obtained show that the PFR is not a fixed and static structure. The pattern of organization of the PFR filament network differs between regions of the flagellum in a straight state and those in a bent state. Measurements of the distances between the PFR filaments and the filaments that connect the PFR to the axoneme as well as of the angles between the intercrossed filaments supported this idea. CONCLUSIONS/SIGNIFICANCE: Graphic computation based on the information obtained allowed the proposal of an animated model for the PFR structure during flagellar beating and provided a new way of observing PFR filaments during flagellar beating. |
| PMID: 20613980 [PubMed - indexed for MEDLINE] | |
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| 6. | Acta Crystallogr Sect F Struct Biol Cryst Commun. 2010 Jul 1;66(Pt 7):862-5. Epub 2010 Jun 26.Protein preparation, crystallization and preliminary X-ray analysis of Trypanosoma cruzi nucleoside diphosphate kinase 1.Gómez Barroso JA, Pereira H, Miranda M, Pereira C, Garratt RC, Aguilar CF.Laboratorio de Biología Molecular Estructural, Instituto Multidisciplinarlo de Investigación en Biología, Universidad Nacional de San Luis and CONICET, Avenida Ejército de los Andes 950, Bloque 1, San Luis, Argentina. AbstractThe flagellated protozoan parasite Trypanosoma cruzi is the aetiological agent of Chagas disease. Nucleoside diphosphate kinases (NDPKs) are enzymes that are involved in energy management and nucleoside balance in the cell. T. cruzi TcNDPK1, a canonical isoform, was overexpressed in Escherichia coli as an N-terminally poly-His-tagged fusion protein and crystallized. Crystals grew after 72 h in 0.2 M MgCl(2), 20% PEG 3350. Data were collected to 3.5 A resolution using synchrotron X-ray radiation at the National Synchrotron Light Laboratory (Campinas, Brazil). The crystals belonged to the trigonal space group P3, with unit-cell parameters a = b = 127.84, c = 275.49 A. Structure determination is under way and will provide relevant information that may lead to the first step in rational drug design for the treatment of Chagas disease. |
| PMID: 20606293 [PubMed - indexed for MEDLINE] | |
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| 7. | Immunobiology. 2010 May;215(5):427-34. Epub 2009 Jul 5.Immunomodulatory effects of zinc and DHEA on the Th-1 immune response in rats infected with Trypano soma cruzi.Brazão V, Santello FH, Caetano LC, Del Vecchio Filipin M, Toldo MP, do Prado JC Jr.Laboratório de Parasitologia, Departamento de Análises Clínicas, Toxicológicas e Bromatológicas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto-Universidade de São Paulo, Avenida do Café s/n, 14040-903 Ribeirão Preto, SP, Brasil. AbstractChagas' disease is considered the sixth most important neglected tropical disease worldwide. Considerable knowledge has been accumulated concerning the role of zinc on cellular immunity. The steroid hormone dehydroepiandrosterone (DHEA) is also known to modulate the immune system. The aims of this paper were to investigate a possible synchronization of their effects on cytokines and NO production and the resistance to Trypanosoma cruzi during the acute phase of infection. It was found that zinc, DHEA or zinc and DHEA supplementation enhanced the immune response, as evidenced by a significant reduction in parasitemia levels. Zinc and DHEA supplementation exerted additive effects on the immune response by elevation of macrophage counts, and by increasing concentrations of IFN-gamma and NO. |
| PMID: 19581019 [PubMed - indexed for MEDLINE] | |
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| 8. | Immunobiology. 2010 May;215(5):413-26. Epub 2009 Jul 5.Proteolytic cleavage of chemokines by Trypanosoma cruzi's cruzipain inhibits ch emokine functions by promoting the generation of antagonists.Benítez-Hernández I, Méndez-Enríquez E, Ostoa P, Fortoul T, Ramírez JA, Stempin C, Cerbán F, Soldevila G, García-Zepeda EA.Departamento de Inmunología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México, D.F. CP. 04510, México. AbstractChagas disease is a chronic inflammatory disease caused by infection with Trypanosoma cruzi. Although it had a decline in recent years, it still affects millions of people in Latin America. The host immune response against this parasite is complex and relies on the development of an efficient T cell-mediated response; however, T. cruzi displays a number of evasion mechanisms allowing it to remain undetected even for years. One of these is the secretion of anti-inflammatory molecules such as proteases and the modulation of biological functions of chemokines. Our objective was to analyze the effect of a major cysteine protease, cruzipain, on a number of critical functions of several CC chemokines, both in vitro and in vivo. Initially, using a murine model of T. cruzi infection, we demonstrated that CCL-2 and CCL-12 chemokines are highly expressed at different stages and correlated with an increase in the expression of cruzipain. In addition, we demonstrated that cruzipain is capable of differentially cleaving CCL-2 and CCL-12 chemokines, as well as CCL-13. Analysis of the proteolysed products identified unique cleavage sites in these chemokines. These cruzipain-modified chemokine products were tested in chemotaxis assays using monocytic cells. We found that cruzipain treated-CCL-2 maintained its biological activity, in contrast to the closely related CCL-12 and CCL-13 chemokines, which showed little or null agonist activity after treatment. Furthermore, based on this analysis, a 14-mer cruzipain-derived chemokine peptide (CDCP-1) was chemically synthesized and tested for agonist activity using in vitro chemotaxis assays. Interestingly, CDCP-1 showed antagonist activity affecting in vitro migration of monocytic cells and calcium flux release. In conclusion, our results demonstrate that cruzipain modulates biological functions of chemokines through proteolytic cleavage, by generating chemokine-derived peptides with antagonist activities. This event could play a role during the latest phases of Chagas disease, when the parasite may differentially modulate chemokine-mediated inflammatory responses. |
| PMID: 19581017 [PubMed - indexed for MEDLINE] | |
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