Saturday, October 3, 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 -7 of 7

1: Sci Signal. 2009 Sep 29;2(90):ra58.

Leishmania GP63 alters host signaling through cleavage-activated protein tyrosine phosphatases.

Gomez MA, Contreras I, Hallé M, Tremblay ML, McMaster RW, Olivier M.

Department of Experimental Medicine, McGill University, Montréal, Québec, Canada.

With more than 12 million people affected worldwide, 2 million new cases occurring per year, and the rapid emergence of drug resistance and treatment failure, leishmaniasis is an infectious disease for which research on drug and vaccine development, host-pathogen, and vector-parasite interactions are current international priorities. Upon Leishmania-macrophage interaction, activation of the protein tyrosine phosphatase (PTP) SHP-1 rapidly leads to the down-regulation of Janus kinase and mitogen-activated protein kinase signaling, resulting in the attenuation of host innate inflammatory responses and of various microbicidal macrophage functions. We report that, in addition to SHP-1, the PTPs PTP1B and TCPTP are activated and posttranslationally modified in infected macrophages, and we identify an essential role for PTP1B in the in vivo progression of Leishmania infection. The mechanism underlying PTP modulation involves the proteolytic activity of the Leishmania surface protease GP63. Access of GP63 to macrophage PTP1B, TCPTP, and SHP-1 is mediated in part by a lipid raft-dependent mechanism, resulting in PTP cleavage and stimulation of phosphatase activity. Collectively, our data present a mechanism of cleavage-dependent activation of macrophage PTPs by an obligate intracellular pathogen and show that internalization of GP63, a key Leishmania virulence factor, into host macrophages is a strategy the parasite uses to interact and survive within its host.

PMID: 19797268 [PubMed - in process]

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2: Infect Immun. 2009 Sep 21. [Epub ahead of print]

Complement Receptor 3-deficiency influences lesion progression during Leishmania major infection in BALB/c mice.

Carter CR, Whitcomb JP, Campbell JA, Mukbel RM, McDowell MA.

Eck Institute for Global Health, Department of Biological Sciences, University of Notre Dame, Notre Dame IN 46556.

Leishmania major is an obligate intracellular protozoan parasite that causes cutaneous leishmaniasis. Like numerous intracellular pathogens, Leishmania exploits cell-surface receptors as a means of entry into host cells. Complement receptor 3 (CR3, CD11b/CD18), a beta2 integrin on phagocytic cells, is one such receptor. Ligation of CR3 has been shown to inhibit production of IL-12, the cytokine pivotal in establishing the cell-mediated response necessary to combat intracellular infection. Here, we investigate the role that CR3 plays in the establishment and progression of cutaneous leishmaniaisis in vivo. Dermal lesions of WT BALB/c are characteristically progressive and lead to extensive tissue necrosis coupled with elevated parasite burdens; CD11b-deficient BALB/c mice, however, demonstrate an intermediate phenotype characterized by chronic lesions, and reduced incidence of tissue damage. Infection followed by re-infection challenge indicates that both susceptible (BALB/c) and resistant (C57Bl/6) mice, regardless of CD11b status, develop resistance to L. major. In addition CD11b does not bias the T helper cytokine response in response to L. major infection. Our results further indicate that CD11b is not necessary for disease resolution in resistant mice; rather this protein appears to play a minor role in susceptibility.

PMID: 19797068 [PubMed - as supplied by publisher]

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3: Med Mal Infect. 2009 Sep 29. [Epub ahead of print]

[No title available]

[Article in French]

Aoun K, Jeddi F, Amri F, Ghrab J, Bouratbine A.

Laboratoire de recherche 05-SP 03 << parasitoses émergentes >>, Tunis, Tunisie; Service de parasitologie-mycologie, Institut Pasteur, 13, place Pasteur, BP 74, 1002 Tunis, Tunisie.

OBJECTIVE: Visceral leishmaniasis is an important health problem in Tunisia. The aim of this study was to update the epidemiological and clinical features of the disease. DESIGN: We performed a retrospective systematic sampling of epidemiological and clinical data collected from the medical records of 1,096 cases of visceral leishmaniasis diagnosed between 1996 and 2006 all over the country. RESULTS: The mean annual incidence of cases was 99.6 cases/year. The mean annual incidence rate was 1.04 cases/100,000 inhabitants, showing an important increase compared to former studies. As expected, children under 5 years (866 cases) were the most affected with a mean annual incidence rate of 9.6 cases/100,000 (p<0.001). The geographical distribution of cases revealed the spreading of the disease from the Northern parts of the country to the Central and even to Southern ones. Rural cases (65.3%) were significantly more numerous than urban ones (34.7%), p<0.001. The sex ratio was 1.03. The diagnostic delay (average of 54 days) was considerably shortened during the study period compared to previous reports, and explains the decrease of the lethality rate (2.9%). CONCLUSIONS: Visceral leishmaniasis has been present in central Tunisia since the early 1990s. Its incidence and the distribution area have increased. This evolution is probably linked to the development of irrigation and agriculture favorable to the multiplication of vector sandflies and dogs reservoirs of Leishmania infantum.

PMID: 19796895 [PubMed - as supplied by publisher]

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4: J Dtsch Dermatol Ges. 2009 Oct;7(s7):s1-s38.

Diagnostik und Therapie der kutanen und mukokutanen Leishmaniasis in Deutschland.

Boecken G, Weitzel T, Sunderkötter C, Fischer M, von Stebut-Borschitz E, Bogdan C, Pietras M, Anders G, Harms-Zwingenberger G, Burchard G, Bialek R, Lippert U, Grobusch M, Erkens K, Fleischer B, Löbermann M, Schunk M, Sterzik B.

Auswärtiges Amt, Gesundheitsdienst, Berlin.

PMID: 19796070 [PubMed - as supplied by publisher]

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5: Parasitology. 2009 Jul;136(8):875-85.Click here to read Nucleotide, Taxonomy via GenBank, Protein, LinkOut

Trypanosoma irwini n. sp (Sarcomastigophora: Trypanosomatidae) from the koala ( Phascolarctos cinereus).

McInnes LM, Gillett A, Ryan UM, Austen J, Campbell RS, Hanger J, Reid SA.

Division of Health Sciences, School of Veterinary and Biomedical Sciences, Murdoch University, Murdoch, Perth 6150, Western Australia. L.Mcinnes@murdoch.edu.au

The morphology and genetic characterization of a new species of trypanosome infecting koalas (Phascolarctos cinereus) are described. Morphological analysis of bloodstream forms and phylogenetic analysis at the 18S rDNA and gGAPDH loci demonstrated this trypanosome species to be genetically distinct and most similar to Trypanosoma bennetti, an avian trypanosome with a genetic distance of 0.9% at the 18S rDNA and 10.7% at the gGAPDH locus. The trypanosome was detected by 18S rDNA PCR in the blood samples of 26 out of 68 (38.2%) koalas studied. The aetiological role of trypanosomes in koala disease is currently poorly defined, although infection with these parasites has been associated with severe clinical signs in a number of koalas. Based on biological and genetic characterization data, this trypanosome species infecting koalas is proposed to be a new species Trypanosome irwini n. sp.

PMID: 19570316 [PubMed - indexed for MEDLINE]

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6: Parasitology. 2009 Jul;136(8):905-18. Epub 2009 Jun 15.Click here to read LinkOut

Involvement of the beta-adrenergic system in the cardiac chronic form of experimental Trypanosoma cruzi infection.

Lo Presti MS, Rivarola HW, Fernández AR, Enders JE, Levin G, Fretes R, Cerban FM, Garrido VV, Paglini-Oliva P.

Cátedra de Física Biomédica, Universidad Nacional de Córdoba. Santa Rosa 1085, Córdoba PC 5000, Argentina. SilviLoPresti@gmail.com

Changes in the cardiac beta-adrenergic system in early stages of Trypanosoma cruzi infection have been described. Here, we studied an early (135 days post-infection-p.i.) and a late stage (365 days p.i.) of the cardiac chronic form of the experimental infection (Tulahuen or SGO-Z12 strains), determining plasma epinephrine and norepinephrine levels, beta-receptor density, affinity and function, cardiac cAMP concentration and phosphodiesterase activity, cardiac contractility, and the presence of beta-receptor autoantibodies. Tulahuen-infected mice presented lower epinephrine and norepinephrine levels; lower beta-receptor affinity and density; a diminished norepinephrine response and higher cAMP levels in the early stage, and a basal contractility similar to non-infected controls in the early and augmented in the late stage. The Tulahuen strain induced autoantibodies with weak beta-receptor interaction. SGO-Z12-infected mice presented lower norepinephrine levels and epinephrine levels that diminished with the evolution of the infection; lower beta-receptor affinity and an increased density; unchanged epinephrine and norepinephrine response in the early and a diminished response in the late stage; higher cAMP levels and unchanged basal contractility. The SGO-Z12 isolate induced beta-receptor autoantibodies with strong interaction with the beta-receptors. None of the antibodies, however, acted a as beta-receptor agonist. The present results demonstrate that this system is seriously compromised in the cardiac chronic stage of T. cruzi infection.

PMID: 19523250 [PubMed - indexed for MEDLINE]

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7: Rev Biol Trop. 2008 Jun;56(2):459-71.LinkOut

[Histometry of the sublingual gland in male and female mice (Mus musculus) infected with the RAL strain of the Chagas parasite, Trypanosoma cruzi]

[Article in Spanish]

de Albuquerque S, Lopes RA, Sala MA, Abrahão AA, Rosa DR.

Departamento de Análisis Clinicos y Bromatológicos, Facultad de Ciencias Farmacéuticas de Ribeirão Preto, USP, Brasil.

The aim of this work was to analyze histologically and histometrically the sublingual gland of mice infected with the RAL strain of T. cruzi, according to the sex. Swiss mice (Mus musculus) were inoculated with 2 x 10(4) blood trypomastigotes of the RAL strain of T. cruzi. In the peak of the parasitemia (12th day) the mice were sacrificed, and the sublingual glands were fixed in ALFAC. HE-stained histological sections were evaluated histometrically. The parasitemia was higher in females. Histopatologically, acini of the infected animals were smaller, with scanty production of secretion, and smaller striated ducts. The nuclei of the demilunes were smaller and showed amastigote nests in the cytoplasm. Karyometrically, nuclei of the acini, demilunes and striated ducts were smaller in the infected mice. Stereologically, it was observed that relative volumes of acini and ducts were smaller and, inversely, relative volumen were greater for the conjunctive tissue in the infected males. The surface densities of acini and ducts were bigger and the diameter and thickness of the wall were smaller in this group. On the other hand, relative volume of acini was smaller and those of the ducts and conjunctive tissue were bigger in the infected females. The diameter and thickness of the wall of acini were smaller, and those of the striated ducts were bigger in this group. The RAL strain of T. cruzi caused general atrophy in the sublingual gland, with numerous nests of parasites in the glandular parenchyma.

PMID: 19256420 [PubMed - indexed for MEDLINE]

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