What's new for 'Trypanosomatids' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

Sender's message:

Sent on Thursday, 2012 February 16
Search: kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"

Click here to view complete results in PubMed (Results may change over time.)
To unsubscribe from these e-mail updates click here.

PubMed Results

Items 1 - 5 of 5

1.	Proc Natl Acad Sci U S A. 2012 Feb 13. [Epub ahead of print] Antigenic diversity is generated by distinct evolutionary mechanisms in African trypanosome species. Jackson AP, Berry A, Aslett M, Allison HC, Burton P, Vavrova-Anderson J, Brown R, Browne H, Corton N, Hauser H, Gamble J, Gilderthorp R, Marcello L, McQuillan J, Otto TD, Quail MA, Sanders MJ, van Tonder A, Ginger ML, Field MC, Barry JD, Hertz-Fowler C, Berriman M. Source Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, United Kingdom. Abstract Antigenic variation enables pathogens to avoid the host immune response by continual switching of surface proteins. The protozoan blood parasite Trypanosoma brucei causes human African trypanosomiasis ("sleeping sickness") across sub-Saharan Africa and is a model system for antigenic variation, surviving by periodically replacing a monolayer of variant surface glycoproteins (VSG) that covers its cell surface. We compared the genome of Trypanosoma brucei with two closely related parasites Trypanosoma congolense and Trypanosoma vivax, to reveal how the variant antigen repertoire has evolved and how it might affect contemporary antigenic diversity. We reconstruct VSG diversification showing that Trypanosoma congolense uses variant antigens derived from multiple ancestral VSG lineages, whereas in Trypanosoma brucei VSG have recent origins, and ancestral gene lineages have been repeatedly co-opted to novel functions. These historical differences are reflected in fundamental differences between species in the scale and mechanism of recombination. Using phylogenetic incompatibility as a metric for genetic exchange, we show that the frequency of recombination is comparable between Trypanosoma congolense and Trypanosoma brucei but is much lower in Trypanosoma vivax. Furthermore, in showing that the C-terminal domain of Trypanosoma brucei VSG plays a crucial role in facilitating exchange, we reveal substantial species differences in the mechanism of VSG diversification. Our results demonstrate how past VSG evolution indirectly determines the ability of contemporary parasites to generate novel variant antigens through recombination and suggest that the current model for antigenic variation in Trypanosoma brucei is only one means by which these parasites maintain chronic infections.
	PMID: 22331916 [PubMed - as supplied by publisher]
	Related citations

2.	Planta Med. 2012 Feb 13. [Epub ahead of print] Cynaropicrin: The First Plant Natural Product with In Vivo Activity against Tr ypanosoma brucei. Zimmermann S, Kaiser M, Brun R, Hamburger M, Adams M. Source Department of Pharmaceutical Sciences, Division of Pharmaceutical Biology, University of Basel, Basel, Switzerland. Abstract A screen of 1800 plant and fungal extracts with subsequent HPLC-based activity profiling was done to identify new antiprotozoal leads from nature. This led to the identification of cynaropicrin (1) from the herb CENTAUREA SALMANTICA L. (Asteraceae) as a potent IN VITRO inhibitor of TRYPANOSOMA BRUCEI RHODESIENSE. It preferentially inhibited T. B. RHODESIENSE (IC (50) of 0.3 µM) and T. BRUCEI GAMBIENSE (IC (50) of 0.2 µM), compared to TRYPANOSOMA CRUZI (IC (50) of 4.4 µM) and PLASMODIUM FALCIPARUM (IC (50) of 3.0 µM). Testing against melarsoprol- and pentamidine-resistant strains (IC (50)s of 0.3 µM and 0.1 µM, respectively) showed no cross-resistance. Intraperitoneal administration of 2 × 10 mg/kg body weight/day in the T. B. RHODESIENSE STIB 900 acute mouse model led to a 92 % reduction of parasitemia compared to untreated controls on day seven post-infection. Removal of the 2-hydroxymethyl-2-propenoyl moiety of cynaropicrin led to a loss of toxicity towards T. B. RHODESIENSE. Cytotoxicities against rat myoblasts (L6 cells), human colon adenocarcinoma cells, and murine peritoneal macrophages were measured, and selectivity indices of 7.8, 62, and 9.5 were determined. This is the first report of a plant natural product with potent IN VIVO activity against TRYPANOSOMA BRUCEI. © Georg Thieme Verlag KG Stuttgart · New York.
	PMID: 22331812 [PubMed - as supplied by publisher]
	Related citations

3.	Molecules. 2012 Feb 13;17(2):1819-29. Chemical and biological analyses of the essential oils and main constituents of piper species. Moura do Carmo DF, Amaral AC, Machado GM, Leon LL, Silva JR. Source Laboratório de Cromatografia, Departamento de Química, Universidade Federal do Amazonas, Av. Rodrigo Otávio, 3000, Coroado, CEP 69077-000, Manaus, AM, Brazil. jrocha_01@yahoo.com.br. Abstract The essential oils obtained from leaves of Piper duckei and Piper demeraranum by hydrodistillation were analyzed by gas chromatography-mass spectrometry. The main constituents found in P. demeraranum oil were limonene (19.3%) and β-elemene (33.1%) and in P. duckei oil the major components found were germacrene D (14.7%) and trans-caryophyllene (27.1%). P. demeraranum and P. duckei oils exhibited biological activity, with IC(50) values between 15 to 76 μg mL-1 against two Leishmania species, P. duckei oil being the most active. The cytotoxicity of the essential oils on mice peritoneal macrophage cells was insignificant, compared with the toxicity of pentamidine. The main mono- and sesquiterpene, limonene (IC(50) = 278 μM) and caryophyllene (IC(50) = 96 μM), were tested against the strains of Leishmania amazonensis, and the IC(50) values of these compounds were lower than those found for the essential oils of the Piper species. The HET-CAM test was used to evaluate the irritation potential of these oils as topical products, showing that these oils can be used as auxiliary medication in cases of cutaneous leishmaniasis, with less side effects and lower costs.
	PMID: 22330429 [PubMed - in process]
	Related citations

4.	Mol Microbiol. 2012 Feb 14. doi: 10.1111/j.1365-2958.2012.08008.x. [Epub ahead of print] The Trypanosoma brucei AIR9-like protein is cytoskeleton-associated and is required for nucleus positioning and accurate cleavage furrow placement. May SF, Peacock L, Almeida Costa CI, Gibson WC, Tetley L, Robinson DR, Hammarton TC. Source Wellcome Trust Centre for Molecular Parasitology, Institute of Infection, Immunity & Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, UK; School of Clinical Veterinary Science, University of Bristol, Langford, Bristol BS40 7DU, UK School of Biological Sciences, University of Bristol, Bristol BS8 1UG, UK Instituto de Higiene e Medicina Tropical, Universidade Nova de Lisboa, Lisbon, Portugal; School of Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK UMR-CNRS 5234, University of Bordeaux, 233076 Bordeaux, France. Abstract AIR9 is a cytoskeleton-associated protein in Arabidopsis thaliana with roles in cytokinesis and cross wall maturation, and reported homologues in land plants and excavate protists, including trypanosomatids. We show that the Trypanosoma brucei AIR9-like protein, TbAIR9, is also cytoskeleton-associated and colocalises with the subpellicular microtubules. We find it to be expressed in all life cycle stages and show that it is essential for normal proliferation of trypanosomes in vitro. Depletion of TbAIR9 from procyclic trypanosomes resulted in increased cell length due to increased microtubule extension at the cell posterior. Additionally, the nucleus was re-positioned to a location posterior to the kinetoplast, leading to defects in cytokinesis and the generation of aberrant progeny. In contrast, in bloodstream trypanosomes, depletion of TbAIR9 had little effect on nucleus positioning, but resulted in aberrant cleavage furrow placement and the generation of non-equivalent daughter cells following cytokinesis. Our data provide insight into the control of nucleus positioning in this important pathogen and emphasise differences in the cytoskeleton and cell cycle control between two life cycle stages of the T. brucei parasite. © 2012 Blackwell Publishing Ltd. © 2012 Blackwell Publishing Ltd.
	PMID: 22329999 [PubMed - as supplied by publisher]
	Related citations

5.	Vet Parasitol. 2011 Sep 27;181(2-4):139-45. Epub 2011 Apr 15. Prolactin: does it exert an up-modulation of the immu ne response in Trypanosoma cruzi-infected rats? Filipin Mdel V, Brazão V, Santello FH, Caetano LC, Toldo MP, do Prado JC Jr. Source Department of Clinical Analysis, Toxicology and Bromatology, College of Pharmaceutical Sciences of Ribeirão Preto (FCFRP), University of São Paulo, Ribeirão Preto, São Paulo, Av. do Café s/n, 14040-903 Ribeirão Preto, SP, Brazil. Abstract During the course of infection by Trypanosoma cruzi, the host immune system is involved in distinct, complex interactions with the endocrine system, and prolactin (PRL) is one of several hormones involved in immunoregulation. Although intensive studies attempting to understand the mechanisms that underlie Chagas' disease have been undertaken, there are still some pieces missing from this complex puzzle. Because data are scarce concerning the role of PRL involvement in Chagas' disease and taking into account the existence of crosstalk between neuroendocrine hormones and the immune system, the current study evaluates a possible up-regulation of the cellular immune response triggered by PRL in T. cruzi-infected rats and the role of PRL in reversing immunosuppression caused by the parasitic infection. The data shown herein demonstrate that PRL induces the proliferation of T lymphocytes, coupled with an activation of macrophages and the production of nitric oxide (NO), leading to a reduction in the number of blood trypomastigotes during the peak of parasitemia. During the acute phase of T. cruzi infection, an enhancement of both CD3+CD4+ and CD3+CD8+ T cell populations were observed in infected groups, with the highest numbers of these T cell subsets found in the infected group treated with PRL. Because NO is a signaling molecule involved in a number of cellular interactions with components of the immune system and the neuroendocrine system, PRL can be considered an alternative hormone able to up-regulate the host's immune system, consequently lowering the pathological effects of a T. cruzi infection. Copyright © 2011 Elsevier B.V. All rights reserved.
	PMID: 21570187 [PubMed - indexed for MEDLINE]
	Related citations