Wednesday, August 26, 2009

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 -10 of 13

1: J Clin Ultrasound. 2009 Aug 24. [Epub ahead of print]Click here to read

Breast involvement in visceral leishmaniasis.

Alimoglu E, Ceken K, Cassano E, Durum Y, Pestereli E.

Department of Radiology, Akdeniz University, Faculty of Medicine, Dumlupinar Bulvari Campus 07059 Arapsuyu, Antalya, Turkey.

Visceral leishmaniasis usually involves the bone marrow, lymph nodes, liver and spleen. Involvement of the eye or respiratory or gastrointestinal systems is very rare and usually occurs in immunodepressed patients. Only one case of breast involvement by protozoa has been reported in the literature. We report a case of a visceral leishmaniasis with a solid breast mass caused by leishmania and diagnosed by sonography-guided core biopsy. (c) 2009 Wiley Periodicals, Inc. J Clin Ultrasound 2009.

PMID: 19705438 [PubMed - as supplied by publisher]

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2: Immunogenetics. 2009 Aug 25. [Epub ahead of print]Click here to read

Distinct genetic control of parasite elimination, dissemination, and disease after Leishmania major infection.

Kurey I, Kobets T, Havelková H, Slapničková M, Quan L, Trtková K, Grekov I, Svobodová M, Stassen AP, Hutson A, Demant P, Lipoldová M.

Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Vídenská 1083, 142 20, Prague 4, Czech Republic.

Elimination of pathogens is the basis of host resistance to infections; however, relationship between persisting pathogens and disease has not been clarified. Leishmania major infection in mice is an important model of host-pathogen relationship. Infected BALB/c mice exhibit high parasite numbers in lymph nodes and spleens, and a chronic disease with skin lesions, splenomegaly, and hepatomegaly, increased serum IgE levels and cytokine imbalance. Although numerous gene loci affecting these disease symptoms have been reported, genes controlling parasites' elimination or dissemination have never been mapped. We therefore compared genetics of the clinical and immunologic symptomatology with parasite load in (BALB/c x CcS-11) F(2) hybrids and mapped five loci, two of which control parasite elimination or dissemination. Lmr5 influences parasite loads in spleens (and skin lesions, splenomegaly, and serum IgE, IL-4, and IFNgamma levels), and Lmr20 determines parasite numbers in draining lymph nodes (and serum levels of IgE and IFNgamma), but no skin or visceral pathology. Three additional loci do not affect parasite numbers but influence significantly the disease phenotype-Lmr21: skin lesions and IFNgamma levels, Lmr22: IL-4 levels, Lmr23: IFNgamma levels, indicating that development of L. major-caused disease includes critical regulations additional to control of parasite spread.

PMID: 19705113 [PubMed - as supplied by publisher]

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3: J Proteomics. 2009 Aug 21. [Epub ahead of print]Click here to read

Proteomic characterization of the released/secreted proteins of Leishmania (Viannia) braziliensis promastigotes.

Cuervo P, De Jesus JB, Saboia-Vahia L, Mendonça-Lima L, Domont GB, Cupolillo E.

Laboratório de Pesquisa em Leishmaniose, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brasil.

Extracellular proteins secreted/released by protozoan parasites are key mediators of the host-parasite interaction. To characterise the profile of proteins secreted/released by Leishmania (Viannia) braziliensis promastigotes, a proteomic approach combining two-dimensional electrophoresis (2DE), tandem matrix-assisted laser desorption ionization-time-of-flight (MALDI-TOF/TOF) mass spectrometry, and data mining was carried out. The 2DE map revealed a set of 270 secreted protein spots from which 42 were confidently identified and classified into 11 categories according to Gene Ontology (GeneDB database) and KEEG Ontology annotation of biological processes. Parasite promastigotes were able to secrete/release proteins involved in immunomodulation, signal transduction, and intracellular survival, such as HSP70, acid phosphatase, activated protein kinase C receptor (LACK), elongation factor 1beta, and tryparedoxin peroxidase. Data mining showed that ~5% of identified proteins present a classical secretion signal whereas ~57% were secreted following non-classical secretion mechanisms, indicating that protein export in this primitive eukaryote might proceed mainly by unconventional pathways. This study reports a suitable approach to identify secreted proteins in the culture supernatant of L. braziliensis and provides new perspectives for the study of molecules potentially involved in the early stages of infection.

PMID: 19703603 [PubMed - as supplied by publisher]

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4: Exp Parasitol. 2009 Aug 21. [Epub ahead of print]Click here to read

Trypanosoma brucei: A putative RNA polymerase II promoter.

Bayele HK.

Department of Structural & Molecular Biology, University College London, Gower Street, London WC1E 6BT, United Kingdom.

RNA polymerase II (pol II) promoters are rare in the African trypanosome Trypanosoma brucei because gene regulation in the parasite is complex and polycistronic. Here we describe a putative pol II promoter and its structure-function relationship. The promoter has features of an archetypal eukaryotic pol II promoter including putative canonical CCAAT and TATA boxes, and an initiator element. However, the spatial arrangement of these elements is only similar to yeast pol II promoters. Deletion mapping and transcription assays enabled delineation of a minimal promoter that could drive orientation-independent reporter gene expression suggesting that it may be a bidirectional promoter. In vitro transcription in a heterologous nuclear extract revealed that the promoter can be recognized by the basal eukaryotic transcription complex. This suggests that the transcription machinery in the parasite may be very similar to those of other eukaryotes.

PMID: 19703444 [PubMed - as supplied by publisher]

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5: Scand J Immunol. 2009 Sep;70(3):226-37.Click here to read

Short-term administration of ethanol in mice deviates antigen presentation activity towards B cells.

Andrade MC, Albernaz MJ, Araújo MS, Santos BP, Teixeira-Carvalho A, Faria AM, Martins-Filho OA.

Laboratório de Biomarcadores de Diagnóstico e Monitoração, Centro de Pesquisas René Rachou, FIOCRUZ, Belo Horizonte, 30190-002 MG, Brazil. marileia@cpqrr.fiocruz.br

Alcohol has a variety of short- and long-term effects on cell-mediated and humoral immune response. Herein, we have characterized the impact of high-dose EtOH administration on phenotypic and functional features of murine APC subsets, including dendritic cell (DC), macrophages and B cells. Impaired cytokine synthesis and Leishmania-phagocytosis was observed in peritoneal macrophages following EtOH administration. Moreover, EtOH exposure led to decreased levels of splenic myeloid DC and increased percentage of macrophages with no changes in splenic lymphoid DC and B cells. Adverse effects of short-term EtOH administration also resulted in impaired OVA-endocytosis by DC and macrophages. In contrast, EtOH consumption upregulates OVA-internalization by B cells. These changes on APC hierarchy may play a role shifting the fate of the immune response after EtOH ingestion. In addition to an overall downregulation of Toll-like receptor-TLR-4 expression by splenic APC, a downregulation of TLR-2 expression in macrophages was observed. Moreover, EtOH exposure altered the expression of co-signalling molecules on splenic APC, downregulating CD40 on macrophages and upregulating CD80 on B cells, with no impact on DC subsets. The net result of changes in TLR-mediated and co-stimulatory signals may determine the altered immunological status induced by acute consumption of alcohol. A direct impact of high-dose EtOH administration in the activation status of splenic CD4(+) T cells was observed. Together, our results demonstrated that short-term high-dose EtOH administration has differential impact on APC populations, downregulating splenic macrophages and DC activity but up-regulating B lymphocyte function as APC, and ultimately yielding a micro-environment that led to increased activation of CD4(+) T cells.

PMID: 19703012 [PubMed - in process]

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6: Int J Dermatol. 2009 Sep;48(9):1027-8.Click here to read

Post-kala-azar dermal leishmaniasis and visceral leishmaniasis in a child--or is it para-kala-azar dermal leishmaniasis?

Mendiratta V, Chander R.

PMID: 19703001 [PubMed - in process]

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7: FEMS Immunol Med Microbiol. 2009 Jul 24. [Epub ahead of print]Click here to read

Common protozoans as an uncommon cause of respiratory ailments in HIV-associated immunodeficiency.

Shankar EM, Vignesh R, Murugavel KG, Balakrishnan P, Ponmalar E, Rao UA, Velu V, Solomon S.

Infectious Diseases Laboratory, YRG Centre for AIDS Research and Education (YRG CARE), Voluntary Health Services Hospital Campus, Chennai, India.

Abstract Opportunistic infections (OIs) are the leading cause of mortality and morbidity among HIV-positive subjects. The breadth of reports of the rare occurrence of OIs in HIV/AIDS has been increasing over the years and more recent studies have outlined the changing trends in the emergence of newer pathogens. Recent reports of the association of certain protozoans that normally do not infect sites other than their normal sites of localization have generated huge interest among scientists. The complete depression of the immune system, followed by the onset of OIs, especially due to protozoans, i.e. toxoplasmosis, isosporiasis, leishmaniasis, cyclosporosis, microsporidiosis and cryptosporidiosis, is not uncommon in AIDS. The immunologic and pathologic basis behind the susceptibility of immunodepressed individuals to these 'non-site-specific parasites' is likely to have a huge impact on HIV disease progression. Certain possible shortcomings in the immunologic armory of immunodeficient subjects, their failure to contain the establishment of these 'uncommon' agents in the human host and their significance in HIV disease progression are discussed.

PMID: 19702877 [PubMed - as supplied by publisher]

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8: Cell Microbiol. 2009 Aug 20. [Epub ahead of print]Click here to read

Differences in human macrophage receptor usage, lysosomal fusion kinetics and survival between logarithmic and metacyclic Leishmania infantum chagasi promastigotes.

Ueno N, Bratt CL, Rodriguez NE, Wilson ME.

VA Medical Center and the Department of Microbiology, the University of Iowa, Iowa City, IA.

Summary The obligate intracellular protozoan, Leishmania infantum chagasi (Lic) undergoes receptor-mediated phagocytosis by macrophages, followed by a transient delay in phagolysosome maturation. We found differences in the pathway through which virulent Lic metacyclic promastigotes or avirulent logarithmic promastigotes are phagocytosed by human monocyte-derived macrophages (MDMs). Both logarithmic and metacyclic promastigotes entered MDMs through a compartment lined by the third complement receptor (CR3). In contrast, many logarithmic promastigotes entered through vacuoles lined by mannose receptors (MR) whereas most metacyclic promastigotes did not (p < 0.005). CR3 positive vacuoles containing metacyclic promastigotes stained for caveolin-1 protein, suggesting CR3 localizes in caveolae during phagocytosis. Following entry, the kinetics of phagolysosomal maturation and intracellular survival also differed. Vacuoles containing metacyclic parasites did not accumulate lysosome-associated membrane protein-1 (LAMP-1) at early times after phagocytosis, whereas vacuoles with logarithmic promastigotes did. MDMs phagocytosed greater numbers of logarithmic than metacyclic promastigotes, yet metacyclics ultimately replicated intracellularly with greater efficiency. These data suggest that virulent metacyclic Leishmania promastigotes fail to ligate macrophage MR, and enter through a path that ultimately enhances intracellular survival. The relatively quiescent entry of virulent Leishmania spp. into macrophages may be accounted for by the ability of metacyclic promastigotes to selectively bypass deleterious entry pathways.

PMID: 19702651 [PubMed - as supplied by publisher]

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9: Proc Natl Acad Sci U S A. 2009 Jul 21;106(29):12133-8. Epub 2009 Jul 8.Click here to read Nucleotide, Taxonomy via GenBank, Protein, LinkOut

Interactions between mutualist Wigglesworthia and tsetse peptidoglycan recognition protein (PGRP-LB) influence trypanosome transmission.

Wang J, Wu Y, Yang G, Aksoy S.

Department of Epidemiology of Microbial Diseases, Yale School of Public Heath, New Haven, CT 06520, USA.

Tsetse flies, the sole vectors of African trypanosomes, have coevolved with mutualistic endosymbiont Wigglesworthia glossinidiae. Elimination of Wigglesworthia renders tsetse sterile and increases their trypanosome infection susceptibility. We show that a tsetse peptidoglycan recognition protein (PGRP-LB) is crucial for symbiotic tolerance and trypanosome infection processes. Tsetse pgrp-lb is expressed in the Wigglesworthia-harboring organ (bacteriome) in the midgut, and its level of expression correlates with symbiont numbers. Adult tsetse cured of Wigglesworthia infections have significantly lower pgrp-lb levels than corresponding normal adults. RNA interference (RNAi)-mediated depletion of pgrp-lb results in the activation of the immune deficiency (IMD) signaling pathway and leads to the synthesis of antimicrobial peptides (AMPs), which decrease Wigglesworthia density. Depletion of pgrp-lb also increases the host's susceptibility to trypanosome infections. Finally, parasitized adults have significantly lower pgrp-lb levels than flies, which have successfully eliminated trypanosome infections. When both PGRP-LB and IMD immunity pathway functions are blocked, flies become unusually susceptible to parasitism. Based on the presence of conserved amidase domains, tsetse PGRP-LB may scavenge the peptidoglycan (PGN) released by Wigglesworthia and prevent the activation of symbiont-damaging host immune responses. In addition, tsetse PGRP-LB may have an anti-protozoal activity that confers parasite resistance. The symbiotic adaptations and the limited exposure of tsetse to foreign microbes may have led to the considerable differences in pgrp-lb expression and regulation noted in tsetse from that of closely related Drosophila. A dynamic interplay between Wigglesworthia and host immunity apparently is influential in tsetse's ability to transmit trypanosomes.

PMID: 19587241 [PubMed - indexed for MEDLINE]

PMCID: PMC2715537 [Available on 2010/01/21]

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10: Genet Mol Res. 2009 Apr 28;8(2):458-76.Click here to read LinkOut

Haplotype distribution of five nuclear genes based on network genealogies and Bayesian inference indicates that Trypanosoma cruzi hybrid strains are polyphyletic.

Tomazi L, Kawashita SY, Pereira PM, Zingales B, Briones MR.

Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, São Paulo, SP, Brasil.

Chagas disease is still a major public health problem in Latin America. Its causative agent, Trypanosoma cruzi, can be typed into three major groups, T. cruzi I, T. cruzi II and hybrids. These groups each have specific genetic characteristics and epidemiological distributions. Several highly virulent strains are found in the hybrid group; their origin is still a matter of debate. The null hypothesis is that the hybrids are of polyphyletic origin, evolving independently from various hybridization events. The alternative hypothesis is that all extant hybrid strains originated from a single hybridization event. We sequenced both alleles of genes encoding EF-1alpha, actin and SSU rDNA of 26 T. cruzi strains and DHFR-TS and TR of 12 strains. This information was used for network genealogy analysis and Bayesian phylogenies. We found T. cruzi I and T. cruzi II to be monophyletic and that all hybrids had different combinations of T. cruzi I and T. cruzi II haplotypes plus hybrid-specific haplotypes. Bootstrap values (networks) and posterior probabilities (Bayesian phylogenies) of clades supporting the monophyly of hybrids were far below the 95% confidence interval, indicating that the hybrid group is polyphyletic. We hypothesize that T. cruzi I and T. cruzi II are two different species and that the hybrids are extant representatives of independent events of genome hybridization, which sporadically have sufficient fitness to impact on the epidemiology of Chagas disease.

PMID: 19551633 [PubMed - indexed for MEDLINE]

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