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Sent on Friday, 2011 Jun 24Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | Drug Test Anal. 2011 Jun;3(6):363-72. doi: 10.1002/dta.229. Epub 2010 Dec 29.Characterization, thermal stability studies, and analytical method development of Paromomycin for formulation development.Khan W, Kumar N.SourceDepartment of Pharmaceutics, National Institute of Pharmaceutical Education & Research (NIPER), Sector 67, S.A.S. Nagar-160062, India. AbstractParomomycin (PM) is an aminoglycoside antibiotic, first isolated in the 1950s, and approved in 2006 for treatment of visceral leishmaniasis. Although isolated six decades back, sufficient information essential for development of pharmaceutical formulation is not available for PM. The purpose of this paper was to determine thermal stability and development of new analytical method for formulation development of PM. PM was characterized by thermoanalytical (DSC, TGA, and HSM) and by spectroscopic (FTIR) techniques and these techniques were used to establish thermal stability of PM after heating PM at 100, 110, 120, and 130 °C for 24 h. Biological activity of these heated samples was also determined by microbiological assay. Subsequently, a simple, rapid and sensitive RP-HPLC method for quantitative determination of PM was developed using pre-column derivatization with 9-fluorenylmethyl chloroformate. The developed method was applied to estimate PM quantitatively in two parenteral dosage forms. PM was successfully characterized by various stated techniques. These techniques indicated stability of PM for heating up to 120 °C for 24 h, but when heated at 130 °C, PM is liable to degradation. This degradation is also observed in microbiological assay where PM lost ∼30% of its biological activity when heated at 130 °C for 24 h. New analytical method was developed for PM in the concentration range of 25-200 ng/ml with intra-day and inter-day variability of < 2%RSD. Characterization techniques were established and stability of PM was determined successfully. Developed analytical method was found sensitive, accurate, and precise for quantification of PM. Copyright © 2010 John Wiley & Sons, Ltd. Copyright © 2010 John Wiley & Sons, Ltd. |
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| 2. | PLoS Pathog. 2011 Jun;7(6):e1002072. Epub 2011 Jun 16.High Affinity Nanobodies against the Trypanosome brucei VSG Are Pote nt Trypanolytic Agents that Block Endocytosis.Stijlemans B, Caljon G, Natesan SK, Saerens D, Conrath K, Pérez-Morga D, Skepper JN, Nikolaou A, Brys L, Pays E, Magez S, Field MC, De Baetselier P, Muyldermans S.SourceLaboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussels, Brussels, Belgium. AbstractThe African trypanosome Trypanosoma brucei, which persists within the bloodstream of the mammalian host, has evolved potent mechanisms for immune evasion. Specifically, antigenic variation of the variant-specific surface glycoprotein (VSG) and a highly active endocytosis and recycling of the surface coat efficiently delay killing mediated by anti-VSG antibodies. Consequently, conventional VSG-specific intact immunoglobulins are non-trypanocidal in the absence of complement. In sharp contrast, monovalent antigen-binding fragments, including 15 kDa nanobodies (Nb) derived from camelid heavy-chain antibodies (HCAbs) recognizing variant-specific VSG epitopes, efficiently lyse trypanosomes both in vitro and in vivo. This Nb-mediated lysis is preceded by very rapid immobilisation of the parasites, massive enlargement of the flagellar pocket and major blockade of endocytosis. This is accompanied by severe metabolic perturbations reflected by reduced intracellular ATP-levels and loss of mitochondrial membrane potential, culminating in cell death. Modification of anti-VSG Nbs through site-directed mutagenesis and by reconstitution into HCAbs, combined with unveiling of trypanolytic activity from intact immunoglobulins by papain proteolysis, demonstrates that the trypanolytic activity of Nbs and Fabs requires low molecular weight, monovalency and high affinity. We propose that the generation of low molecular weight VSG-specific trypanolytic nanobodies that impede endocytosis offers a new opportunity for developing novel trypanosomiasis therapeutics. In addition, these data suggest that the antigen-binding domain of an anti-microbial antibody harbours biological functionality that is latent in the intact immunoglobulin and is revealed only upon release of the antigen-binding fragment. |
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| 3. | PLoS One. 2011;6(6):e20568. Epub 2011 Jun 17.The IFN-γ-Inducible GTPase, Irga6, Protects Mice against Toxoplasma gondii but Not against Plasmodium berghei and Some Other Intracellular Pathogens.Liesenfeld O, Parvanova I, Zerrahn J, Han SJ, Heinrich F, Muñoz M, Kaiser F, Aebischer T, Buch T, Waisman A, Reichmann G, Utermöhlen O, von Stebut E, von Loewenich FD, Bogdan C, Specht S, Saeftel M, Hoerauf A, Mota MM, Könen-Waisman S, Kaufmann SH, Howard JC.SourceInstitute of Microbiology and Hygiene, Charité Universitätsmedizin Berlin, Berlin, Germany. AbstractClearance of infection with intracellular pathogens in mice involves interferon-regulated GTPases of the IRG protein family. Experiments with mice genetically deficient in members of this family such as Irgm1(LRG-47), Irgm3(IGTP), and Irgd(IRG-47) has revealed a critical role in microbial clearance, especially for Toxoplasma gondii. The in vivo role of another member of this family, Irga6 (IIGP, IIGP1) has been studied in less detail. We investigated the susceptibility of two independently generated mouse strains deficient in Irga6 to in vivo infection with T. gondii, Mycobacterium tuberculosis, Leishmania mexicana, L. major, Listeria monocytogenes, Anaplasma phagocytophilum and Plasmodium berghei. Compared with wild-type mice, mice deficient in Irga6 showed increased susceptibility to oral and intraperitoneal infection with T. gondii but not to infection with the other organisms. Surprisingly, infection of Irga6-deficient mice with the related apicomplexan parasite, P. berghei, did not result in increased replication in the liver stage and no Irga6 (or any other IRG protein) was detected at the parasitophorous vacuole membrane in IFN-γ-induced wild-type cells infected with P. berghei in vitro. Susceptibility to infection with T. gondii was associated with increased mortality and reduced time to death, increased numbers of inflammatory foci in the brains and elevated parasite loads in brains of infected Irga6-deficient mice. In vitro, Irga6-deficient macrophages and fibroblasts stimulated with IFN-γ were defective in controlling parasite replication. Taken together, our results implicate Irga6 in the control of infection with T. gondii and further highlight the importance of the IRG system for resistance to this pathogen. |
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| 4. | Int J Infect Dis. 2011 Jun 20. [Epub ahead of print]Clinicopathological features and the practice of diagnosing infectious cutaneous granulomas in Egypt.< /a>El-Khalawany M, Meraag I, Eassa B, El-Naby HH.SourceDepartment of Dermatology and Venereology, Al-Hussein University Hospital, Al-Azhar University, Box 32515, Al-Darasah, Cairo, Egypt. AbstractOBJECTIVE:To present the clinicopathological features and the practice of diagnosing infectious cutaneous granulomas in Egypt. METHODS:This study included all cases diagnosed with infectious cutaneous granuloma during the period 2004-2010 at Al-Hussein University Hospital, Cairo. Clinical and histological features were recorded, along with the positivity rate (PR) for each diagnostic method. RESULTS:This study included 233 cases (150 males and 83 females) with a mean age of 47 years. Three groups of infection were recorded: bacterial infections (73.8% Mycobacterium and 3.9% non-Mycobacterium), parasitic infestations (16.7%), and deep fungal infections (5.6%). Tuberculosis cases formed the largest granuloma group (40.8%), followed by leprosy (31.7%) and leishmaniasis (15.9%). A total of 36 cases were diagnosed by direct smear (PR 15.5%), 61 cases by skin biopsy (PR 31.0%), 84 cases by intradermal test (PR 63.6%), 26 cases by serological tests (PR 60.5%), 18 cases by tissue culture (PR 69.2%), and eight cases by PCR (PR 100%). CONCLUSIONS:Mycobacterial infections constitute the most common infectious cutaneous granulomas among Egyptians. Routine methods such as direct smear, skin biopsy, and intradermal tests remain the most commonly applied and economical methods for diagnosis in developing countries, although specific methods such as tissue culture and PCR have higher positivity rates in the diagnosis. Copyright © 2011 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved. |
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| 5. | Infect Immun. 2011 May;79(5):2112-9. Epub 2011 Mar 14.Type I interferons increase host susceptibility to Trypanosoma cruzi infection.< /a>Chessler AD, Caradonna KL, Da'dara A, Burleigh BA.SourceDepartment of Immunology and Infectious Diseases, Harvard School of Public Health, Building I, Rm. 817, 665 Huntington Avenue, Boston, MA 02115, USA. AbstractTrypanosoma cruzi, the protozoan parasite that causes human Chagas' disease, induces a type I interferon (IFN) (IFN-α/β) response during acute experimental infection in mice and in isolated primary cell types. To examine the potential impact of the type I IFN response in shaping outcomes in experimental T. cruzi infection, groups of wild-type (WT) and type I IFN receptor-deficient (IFNAR(-/-)) 129sv/ev mice were infected with two different T. cruzi strains under lethal and sublethal conditions and several parameters were measured during the acute stage of infection. The results demonstrate that type I IFNs are not required for early host protection against T. cruzi. In contrast, under conditions of lethal T. cruzi challenge, WT mice succumbed to infection whereas IFNAR(-/-) mice were ultimately able to control parasite growth and survive. T. cruzi clearance in and survival of IFNAR(-/-) mice were accompanied by higher levels of IFN-γ production by isolated splenocytes in response to parasite antigen. The suppression of IFN-γ in splenocytes from WT mice was independent of IL-10 levels. While the impact of type I IFNs on the production of IFN-γ and other cytokines/chemokines remains to be fully determined in the context of T. cruzi infection, our data suggest that, under conditions of high parasite burden, type I IFNs negatively impact IFN-γ production, initiating a detrimental cycle that contributes to the ultimate failure to control infection. These findings are consistent with a growing theme in the microbial pathogenesis field in which type I IFNs can be detrimental to the host in a variety of nonviral pathogen infection models. |
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| 6. | Infect Immun. 2011 May;79(5):2120-30. Epub 2011 Feb 28.Heterologous plasmid DNA prime-recombinant human adenovirus 5 boost vaccination generates a stable pool of protective long-lived CD8(+) T effector memory cells specific for a human parasite, Trypanosoma cruzi.Rigato PO, de Alencar BC, de Vasconcelos JR, Dominguez MR, Araújo AF, Machado AV, Gazzinelli RT, Bruna-Romero O, Rodrigues MM.SourceCTCMol, UNIFESP, Escola Paulista de Medicina, Rua Mirassol 207, São Paulo, SP, Brazil 04044-010. AbstractRecently, we described a heterologous prime-boost strategy using plasmid DNA followed by replication-defective human recombinant adenovirus type 5 as a powerful strategy to elicit long-lived CD8(+) T-cell-mediated protective immunity against experimental systemic infection of mice with a human intracellular protozoan parasite, Trypanosoma cruzi. In the present study, we further characterized the protective long-lived CD8(+) T cells. We compared several functional and phenotypic aspects of specific CD8(+) T cells present 14 or 98 days after the last immunizing dose and found the following: (i) the numbers of specific cells were similar, as determined by multimer staining or by determining the number of gamma interferon (IFN-γ)-secreting cells by enzyme-linked immunospot (ELISPOT) assay; (ii) these cells were equally cytotoxic in vivo; (iii) following in vitro stimulation, a slight decline in the frequency of multifunctional cells (CD107a(+) IFN-γ(+) or CD107a(+) IFN-γ(+) tumor necrosis factor alpha positive [TNF-α(+)]) was paralleled by a significant increase of CD107a singly positive cells after 98 days; (iv) the expression of several surface markers was identical, except for the reexpression of CD127 after 98 days; (v) the use of genetically deficient mice revealed a role for interleukin-12 (IL-12)/IL-23, but not IFN-γ, in the maintenance of these memory cells; and (vi) subsequent immunizations with an unrelated virus or a plasmid vaccine or the depletion of CD4(+) T cells did not significantly erode the number or function of these CD8(+) T cells during the 15-week period. From these results, we concluded that heterologous plasmid DNA prime-adenovirus boost vaccination generated a stable pool of functional protective long-lived CD8(+) T cells with an effector memory phenotype. |
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| 7. | Infect Immun. 2011 May;79(5):1873-81. Epub 2011 Feb 28.Regulation of Trypanosoma cruzi-induced myocarditis by programmed death cell receptor 1.Gutierrez FR, Mariano FS, Oliveira CJ, Pavanelli WR, Guedes PM, Silva GK, Campanelli AP, Milanezi CM, Azuma M, Honjo T, Teixeira MM, Aliberti JC, Silva JS.SourceDepartment of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, USP Av. Bandeirantes, 3900 Ribeirão Preto, São Paulo 14049-900, Brazil. AbstractTrypanosoma cruzi infection causes intense myocarditis, leading to cardiomyopathy and severe cardiac dysfunction. Protective adaptive immunity depends on balanced signaling through a T cell receptor and coreceptors expressed on the T cell surface. Such coreceptors can trigger stimulatory or inhibitory signals after binding to their ligands in antigen-presenting cells (APC). T. cruzi modulates the expression of coreceptors in lymphocytes after infection. Deregulated inflammation may be due to unbalanced expression of these molecules. Programmed death cell receptor 1 (PD-1) is a negative T cell coreceptor that has been associated with T cell anergy or exhaustion and persistent intracellular infections. We aimed to study the role of PD-1 during T. cruzi-induced acute myocarditis in mice. Cytometry assays showed that PD-1 and its ligands are strongly upregulated in lymphocytes and APC in response to T. cruzi infection in vivo and in vitro. Lymphocytes infiltrating the myocardium exhibited high levels of expression of these molecules. An increased cardiac inflammatory response was found in mice treated with blocking antibodies against PD-1, PD-L1, and to a lesser extent, PD-L2, compared to that found in mice treated with rat IgG. Similar results in PD-1(-/-) mice were obtained. Moreover, the PD-1 blockade/deficiency led to reduced parasitemia and tissue parasitism but increased mortality. These results suggest the participation of a PD-1 signaling pathway in the control of acute myocarditis induced by T. cruzi and provide additional insight into the regulatory mechanisms in the pathogenesis of Chagas' disease. |
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| 8. | Infect Immun. 2011 May;79(5):1855-62. Epub 2011 Feb 22.Trypanosoma cruzi infection induces a global host cell respo nse in cardiomyocytes.Manque PA, Probst C, Pereira MC, Rampazzo RC, Ozaki LS, Pavoni DP, Silva Neto DT, Carvalho MR, Xu P, Serrano MG, Alves JM, Meirelles Mde N, Goldenberg S, Krieger MA, Buck GA.SourceDepartment of Microbiology, Virginia Commonwealth University, Richmond, VA, USA. AbstractChagas' disease, caused by the hemoflagellate protozoan Trypanosoma cruzi, affects millions of people in South and Central America. Chronic chagasic cardiomyopathy, the most devastating manifestation of this disease, occurs in approximately one-third of infected individuals. Events associated with the parasite's tropism for and invasion of cardiomyocytes have been the focus of intense investigation in recent years. In the present study, we use murine microarrays to investigate the cellular response caused by invasion of primary murine cardiomyocytes by T. cruzi trypomastigotes. These studies identified 353 murine genes that were differentially expressed during the early stages of invasion and infection of these cells. Genes associated with the immune response, inflammation, cytoskeleton organization, cell-cell and cell-matrix interactions, apoptosis, cell cycle, and oxidative stress are among those affected during the infection. Our data indicate that T. cruzi induces broad modulations of the host cell machinery in ways that provide insight into how the parasite survives, replicates, and persists in the infected host and ultimately defines the clinical outcome of the infection. |
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