What's new for 'Trypanosomatids' in PubMed

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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 -3 of 3

1: PLoS One. 2009 Oct 12;4(10):e7420.

Searching for New Clues about the Molecular Cause of Endomyocardial Fibrosis by Way of In Silico Proteomics and Analytical Chemistry.

Wayengera M.

Division of Molecular Pathology, Department of Pathology, School of Biomedical Sciences, College of Health Sciences, Makerere University, Kampala, Uganda.

BACKGROUND: Endomyocardial Fibrosis (EMF) -is a chronic inflammatory disease of the heart with related pathology to that of late stage Chaga's disease. Indeed, both diseases are thought to result from auto-immune responses against myocardial tissue. As is the case that molecular mimicry between the acidic termini of Trypanosoma cruzi ribosomal P0, P1 and P2beta (or simply TcP0, TcP1, and TcP2beta) proteins and myocardial tissue causes Chaga's disease, excessive exposure to certain infections, toxins including cassava ones, allergy and malnutrition has been suggested as the possible cause for EMF. Recent studies have defined the proteomic characteristics of the T. cruzi ribosomal P protein-C-termini involved in mediating auto-immunity against Beta1-adrenergic receptors of the heart in Chaga's disease. This study aimed to investigate the similarity of C-termini of TcP0/TcP2beta to sequences and molecules of several plants, microbial, viral and chemical elements- most prior thought to be possible causative agents for EMF. METHODS AND PRINCIPAL FINDINGS: Comparative Sequence alignments and phylogeny using the BLAST-P tool at the Swiss Institute of Biotechnology (SIB) revealed homologs of C-termini of TcP0 and TcP2beta among related proteins from several eukaryotes including the animals (Homo sapiens, C. elegans, D. melanogaster), plants (Arabidopsis thaliana, Zea mays, Glycina Max, Oryza sativa, Rhizopus oryzae) and protozoa (P. falciparum, T. gondii, Leishmania spp).The chemical formulae of the two T.cruzi ribosomal protein C-terminal peptides were found to be C(61)H(83)N(13)O(26)S(1)and C(64)H(87)N(13)O(28)S(1) respectively by Protparam. Both peptides are heavily negatively charged. Constitutively, both auto-antigens predominantly contain Asparagine (D), Glycine (G) and Phenylamine (F), with a balanced Leucine (L) and Methionine (M) percent composition of 7.7%. The afore going composition, found to be non-homologous to all molecules of chemical species in the databases searched, suggests the possible role of a metabolic pathway in the pathogenesis of EMF if aligned with our "molecular mimicry" hypothesis. CONCLUSIONS: Our findings provide a "window" to suggest that cross reactivity of antibodies against C-terminal sequences of several animal, plant and protozoal ribosomal P proteins with heart tissue may mediate EMF in a similar manner as C- termini of T. cruzi do for Chaga's disease.

PMID: 19823676 [PubMed - in process]

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• Trypanosoma cruzi acidic ribosomal P protein gene family. Novel P proteins encoding unusual cross-reactive epitopes.

  J Immunol. 1993 Nov 15; 151(10):5504-15.

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• Antigens shared by Leishmania species and Trypanosoma cruzi: immunological comparison of the acidic ribosomal P0 proteins.

  Infect Immun. 1994 May; 62(5):1643-51.

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• Antibodies against the carboxyl-terminal end of the Trypanosoma cruzi ribosomal P proteins are pathogenic.

  FASEB J. 2001 Dec; 15(14):2602-12.

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• ReviewHumoral autoimmune response in Chagas' disease: Trypanosoma cruzi ribosomal antigens as immunizing agents.

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2: Antimicrob Agents Chemother. 2009 Oct 12. [Epub ahead of print]

Comparative efficacy of two antimony regimens to treat Leishmania braziliensis-induced cutaneous leishmaniasis in rhesus macaques (Macaca mulatta).

Grimaldi G Jr, Porrozzi R, Friedrich K, Teva A, Marchevsky RS, Vieira F, Miekeley N, Paumgartten FJ.

Laboratório de Pesquisa em Leishmaniose, Instituto Oswaldo Cruz, Laboratório de Toxicologia Ambiental, Escola Nacional de Saúde Pública, Laboratório de Neurovirulência, Instituto de Tecnologia em Imunobiológicos, Fiocruz; and Departamento de Química, Pontifícia Universidade Católica do Rio de Janeiro, Rio de Janeiro, Brazil.

This study compares the efficacy of two N-methylglucomine antimoniate (MA) dose regimens for treating macaques with L. braziliensis-induced chronic skin disease. Whereas all animals treated with the full dose (20 mg MA/kg/day) were cured, 50% of monkeys receiving a low dose (5 mg MA/kg/day) regimen relapsed. The antimony concentrations in macaque plasma and tissue samples were greater in the full dose group compared to macaques receiving a sub-therapeutic MA regimen. Our data also suggest the presence of drug-induced hepatic pathology.

PMID: 19822700 [PubMed - as supplied by publisher]

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• Responses of Leishmania (Viannia) braziliensis cutaneous infection to N-methylglucamine antimoniate in the rhesus monkey (Macaca mulatta) model.

  J Parasitol. 2005 Aug; 91(4):976-8.

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• Cross-immunity experiments between different species or strains of Leishmania in rhesus macaques (Macaca mulatta).

  Am J Trop Med Hyg. 2004 Sep; 71(3):297-305.

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• A comparative study between the efficacy of systemic meglumine antimoniate therapy with standard or low dose plus oral omeprazole in the treatment of cutaneous leishmaniasis.

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• ReviewInterventions for American cutaneous and mucocutaneous leishmaniasis.

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3: Infect Immun. 2009 Oct;77(10):4383-95. Epub 2009 Aug 3. LinkOut

Perforin and gamma interferon expression are required for CD4+ and CD8+ T-cell-dependent protective immunity against a human parasite, Trypanosoma cruzi, elicited by heterologous plasmid DNA prime-recombinant adenovirus 5 boost vaccination.

de Alencar BC, Persechini PM, Haolla FA, de Oliveira G, Silverio JC, Lannes-Vieira J, Machado AV, Gazzinelli RT, Bruna-Romero O, Rodrigues MM.

Centro Interdisciplinar de Terapia Gênica (CINTERGEN), Universidade Federal de São Paulo-Escola Paulista de Medicina, Rua Mirassol 207, São Paulo, SP 04044-010, Brazil.

A heterologous prime-boost strategy using plasmid DNA, followed by replication-defective recombinant adenovirus 5, is being proposed as a powerful way to elicit CD4(+) and CD8(+) T-cell-mediated protective immunity against intracellular pathogens. We confirmed this concept and furthered existing research by providing evidence that the heterologous prime-boost regimen using the gene encoding amastigote surface protein 2 elicited CD4(+) and CD8(+) T-cell-mediated protective immunity (reduction of acute parasitemia and prolonged survival) against experimental infection with Trypanosoma cruzi. Protective immunity correlated with the presence of in vivo antigen-specific cytotoxic activity prior to challenge. Based on this, our second goal was to determine the outcome of infection after heterologous prime-boost immunization of perforin-deficient mice. These mice were highly susceptible to infection. A detailed analysis of the cell-mediated immune responses in immunized perforin-deficient mice showed an impaired gamma interferon (IFN-gamma) secretion by immune spleen cells upon restimulation in vitro with soluble recombinant antigen. In spite of a normal numeric expansion, specific CD8(+) T cells presented several functional defects detected in vivo (cytotoxicity) and in vitro (simultaneous expression of CD107a/IFN-gamma or IFN-gamma/tumor necrosis factor alpha) paralleled by a decreased expression of CD44 and KLRG-1. Our final goal was to determine the importance of IFN-gamma in the presence of highly cytotoxic T cells. Vaccinated IFN-gamma-deficient mice developed highly cytotoxic cells but failed to develop any protective immunity. Our study thus demonstrated a role for perforin and IFN-gamma in a number of T-cell-mediated effector functions and in the antiparasitic immunity generated by a heterologous plasmid DNA prime-adenovirus boost vaccination strategy.

PMID: 19651871 [PubMed - indexed for MEDLINE]

PMCID: PMC2747960 [Available on 2010/04/01]

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  Infect Immun. 1999 Aug; 67(8):3855-63.

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