Tuesday, April 7, 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 20

1: J Vet Med Sci. 2009 Mar;71(3):313-8.

Both Type-I and Type-II Responses Contribute to Murine Trypanotolerance.

Namangala B, DE Baetselier P, Beschin A.

The University of Zambia, Faculty of Veterinary Medicine, Department of Paraclinical Studies.

The host immune system has been documented to influence the course and outcome of infection with the phospholipase-C-deficient (PLC(-/-)) Trypanosoma brucei brucei. We addressed the resistant mechanisms during trypanosomosis by comparing the immune response to variant-specific surface glycoprotein (VSG) in relatively susceptible C3H mice and trypanotolerant (C57BL/6 x BALB/c)-F1 (B6B-F1) mice infected with PLC(-/-) parasites. During the early stage of infection, lymphoid cells from both PLC(-/-)-susceptible C3H and -tolerant B6B-F1 mice mainly secreted VSG-specific IFN-gamma. Although C3H mice remained locked in a type-I cytokine environment (IFN-gamma, TNF-alpha) during late stage of infection, B6B-F1 mice switched to production of type-II cytokines (IL-4, IL-10) from late stage of infection onwards. It seems that VSG-specific cytokine responses associated with resistance to murine African trypanosomosis are infection-stage dependent, with type-I cytokine responses being critical during the early stage of infection while type-II cytokine responses appear to be more important during the late and chronic phases of the disease. Because of the striking similarities in the course of the PLC(-/-)infection in B6B-F1 mice with that of the trypanotolerant N'dama cattle naturally-infected with T. congolense, the PLC(-/-)-infected B6B-F1 mice represents a suitable model to study the course of infection and immune responses during bovine trypanosomosis.

PMID: 19346699 [PubMed - in process]

2: Mol Cell Proteomics. 2009 Apr 4. [Epub ahead of print]Click here to read

The phosphoproteome of bloodstream form trypanonosoma brucei, causative agent of African sleeping sickness.

Nett IR, Martin DM, Miranda-Saavedra D, Lamont D, Barber JD, Mehlert A, Ferguson MA.

Division of Biological Chemistry & Drug Discovery, University of Dundee, Dundee, Scotland DD1 5EH.

The protozoan parasite Trypanosoma brucei is the causative agent of human African sleeping sickness and related animal diseases and it has over 170 predicted protein kinases. Protein phosphorylation is a key regulatory mechanism for cellular function that, thus far, has been studied in T. brucei principally through putative kinase mRNA knockdown and observation of the resulting phenotype. However, despite the relatively large kinome of this organism, and the demonstrated essentiality of several T. brucei kinases, only 8 specific phosphorylation sites have been determined in this organism. Using a gel-free, phosphopeptide-enrichment, based proteomics approach we have performed the first large-scale phosphorylation site analyses for T. brucei. Serine, threonine and tyrosine phosphorylation sites were determined for a cytosolic protein fraction of the bloodstream form of the parasite, resulting in the identification of 491 phosphoproteins based on the identification of 852 unique phosphopeptides and 1204 phosphorylation sites. The phosphoproteins detected in this study are predicted from their genome annotations to participate in a wide variety of biological processes, including signal transduction, processing of DNA and RNA, protein synthesis and degradation and to a minor extent in metabolic pathways. The analysis of phoshopeptides and phosphorylation sites was facilitated by in-house developed software and this automated approach was validated by manual annotation of spectra of the kinase subset of proteins. Analysis of the cytosolic bloodstream form T. brucei kinome revealed the presence of 44 phosphorylated protein kinases in our dataset, which could be classified into the major eukaryotic protein kinase groups by applying a multi-level hidden Markov model (HMM) library of the kinase catalytic domain. Identification of the kinase phosphorylation sites showed conserved phosphorylation sequence motifs in several kinase activation segments, which supports the view that phosphorylation-based signalling is a general and fundamental regulatory process that extends to this highly divergent lower eukaryote.

PMID: 19346560 [PubMed - as supplied by publisher]

3: Vet Rec. 2009 Apr 4;164(14):433-4.Click here to read

Effects of therapy on haemostasis in dogs infected with Leishmania infantum, Ehrlichia canis, or both combined.

Cortese L, Pelagalli A, Piantedosi D, Cestaro A, Di Loria A, Lombardi P, Avallone L, Ciaramella P.

Dipartimento di Scienze Cliniche Veterinarie - Sezione di Clinica Medica, Facoltà di Medicina Veterinaria, Università degli Studi di Napoli Federico II, Via F. Delpino 1, 80137 Napoli, Italy.

PMID: 19346544 [PubMed - in process]

4: J Antimicrob Chemother. 2009 Apr 4. [Epub ahead of print]Click here to read

Nitazoxanide, tizoxanide and a new analogue [4-nitro-N-(5-nitro-1,3-thiazol-2-yl)benzamide; NTB] inhibit the growth of kinetoplastid parasites (Trypanosoma cruzi and Leishmania mexicana) in vitro.

Chan-Bacab MJ, Hernández-Núñez E, Navarrete-Vázquez G.

Departamento de Microbiología Ambiental y Biotecnología, Universidad Autónoma de Campeche, Campeche 24030, México.

PMID: 19346519 [PubMed - as supplied by publisher]

Patient Drug Information

  • Nitazoxanide (Alinia® )

    Nitazoxanide is used to treat diarrhea in children and adults caused by the protozoaCryptosporidium orGiardia. Protozoa are suspected as the cause when diarrhea lasts more than 7 days. Nitazoxanide is in a class of medic...

  • Source: AHFS Consumer Medication Information
5: Proc Natl Acad Sci U S A. 2009 Apr 3. [Epub ahead of print]Click here to read

Leishmania amazonensis promastigotes induce and are killed by neutrophil extracellular traps.

Guimarães-Costa AB, Nascimento MT, Froment GS, Soares RP, Morgado FN, Conceição-Silva F, Saraiva EM.

Departamento de Imunologia, Instituto de Microbiologia Prof. Paulo de Góes, Universidade Federal do Rio de Janeiro, Bloco I, 21941-902, Rio de Janeiro, Brazil;

Neutrophils are short-lived leukocytes that die by apoptosis, necrosis, and NETosis. Upon death by NETosis, neutrophils release fibrous traps of DNA, histones, and granule proteins named neutrophil extracellular traps (NETs), which can kill bacteria and fungi. Inoculation of the protozoan Leishmania into the mammalian skin causes local inflammation with neutrophil recruitment. Here, we investigated the release of NETs by human neutrophils upon their interaction with Leishmania parasites and NETs' ability to kill this protozoan. The NET constituents DNA, elastase, and histones were detected in traps associated to promastigotes by immunofluorescence. Electron microscopy revealed that Leishmania was ensnared by NETs released by neutrophils. Moreover, Leishmania and its surface lipophosphoglycan induced NET release by neutrophils in a parasite number- and dose-dependent manner. Disruption of NETs by DNase treatment during Leishmania-neutrophil interaction increased parasite survival, evidencing NETs' leishmanicidal effect. Leishmania killing was also elicited by NET-rich supernatants from phorbol 12-myristate 13-acetate-activated neutrophils. Immunoneutralization of histone during Leishmania-neutrophil interaction partially reverted Leishmania killing, and purified histone killed the parasites. Meshes composed of DNA and elastase were evidenced in biopsies of human cutaneous leishmaniasis. NET is an innate response that might contribute to diminish parasite burden in the Leishmania inoculation site.

PMID: 19346483 [PubMed - as supplied by publisher]

6: Am J Trop Med Hyg. 2009 Apr;80(4):593-5.Click here to read

First report of Lutzomyia (Nyssomyia) neivai (Diptera: Psychodidae: Phlebotominae) naturally infected by Leishmania (Viannia) braziliensis in a Periurban area of south Brazil using a multiplex polymerase chain reaction assay.

Pita-Pereira D, Souza GD, Zwetsch A, Alves CR, Britto C, Rangel EF.

Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, RJ, Brasil.

To identify Lutzomyia (Nyssomyia) neivai naturally infected by Leishmania a multiplex polymerase chain reaction (PCR) was used for the analysis of 450 specimens (270 females, 180 males) collected in an endemic periurban area of cutaneous leishmaniasis in Porto Alegre, Brazil. Insects were grouped into pools of 10 and positive results were achieved in 3/27 Lu. (N.) neivai female pools. Infection by L. (Viannia) braziliensis was confirmed after hybridizing PCR products with a subgenus-specific biotinylated probe. Considering the detection of three positive pools with at least one infected insect in each, an infection rate of 1.1% was estimated. Our results associated with epidemiologic data suggest a potential ability of Lu. (N.) neivai in transmitting L. braziliensis in Porto Alegre, where the first notifications of autochthonous cutaneous leishmaniasis in humans occurred in 2002, with an increase in the number of cases in recent years possibly as a consequence of deforestation and agricultural activities in the area.

PMID: 19346382 [PubMed - in process]

7: Am J Trop Med Hyg. 2009 Apr;80(4):580-2.Click here to read

Relapse of visceral leishmaniasis after miltefosine treatment in a Nepalese patient.

Pandey BD, Pandey K, Kaneko O, Yanagi T, Hirayama K.

Sukraraj Tropical and Infectious Diseases Hospital, Kathmandu, Nepal.

We report the first case of visceral leishmaniasis (VL) relapse in a healthy individual after complete miltefosine treatment. The patient attended hospital with a history of fever for 2 months, splenomegaly, hepatomegaly, and weight loss. The case was confirmed as VL by microscopical detection of Leishmania parasites in a bone marrow specimen and by a positive result for the immunochromatography-based test targeting the Leishmania donovani rK39 antibody. A polymerase chain reaction (PCR) specific for the Leishmania kinetoplast minicircle gene was positive, and subsequent sequencing of the PCR-amplified product confirmed that this case was a L. donovani infection. The patient was treated with miltefosine for 28 days, during which time the response was good, and the Leishman-Donovan body (LD body) was negative on discharge. Ten months later, however, this patient again developed high fever and splenomegaly, and LD bodies and rK39 antibody were positive, thus indicating a relapse of VL. The patient was subsequently treated with 1 mg/kg of amphotericin B for a total of 14 days and recovered completely.

PMID: 19346379 [PubMed - in process]

8: Am J Trop Med Hyg. 2009 Apr;80(4):574-9.Click here to read

Association of treatment of American cutaneous leishmaniasis prior to ulcer development with high rate of failure in northeastern Brazil.

Unger A, O'Neal S, Machado PR, Guimarães LH, Morgan DJ, Schriefer A, Bacellar O, Glesby MJ, Carvalho EM.

Departments of Medicine and Pediatrics, University of California, Los Angeles, USA.

Cure rates for American cutaneous leishmaniasis (ACL) range between 60% and 90%. Early evidence suggests lower cure rates for early ACL before the development of the ulceration. We evaluated risk factors for treatment failure in patients with early and classic ulcerative ACL. Patients (n = 136) were 13-60 years of age and had lesions with a duration of 15-90-days. Patients were treated with antimony (20 mg/kg/day for 20 days). The primary outcome was lesion cure by 90 days without recurrence. Patients with early ACL (n = 16) had papules, nodules, plaques, or superficial ulcerations with less than 30 days of illness. Patients with classic ulcerative ACL (n = 120) had ulcerated classic lesions, longer duration, larger lesions, and higher levels of interferon-gamma and tumor necrosis factor-alpha (P < or = 0.01 for all comparisons). Ulcerated lesions were associated with a lower treatment failure rate compared with early ACL (25.8% versus 75.0%; P < 0.001). Early treatment of ACL does not prevent lesion ulceration and is associated with higher rates of treatment failure.

PMID: 19346378 [PubMed - in process]

Patient Drug Information

9: Am J Trop Med Hyg. 2009 Apr;80(4):568-73.Click here to read

Effect of oral treatment with pyrazole carbohydrazide derivatives against murine infection by Leishmania amazonensis.

Charret KS, Rodrigues RF, Bernardino AM, Gomes AO, Carvalho AV, Canto-Cavalheiro MM, Leon L, Amaral VF.

Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil.

Newly synthesized pyrazole carbohydrazide derivatives with substituents X = Br/Y = NO(2) and X = NO(2)/Y = Cl were independently investigated in the CBA mouse model of cutaneous leishmaniasis. Animals were infected with Leishmania amazonensis and treated two weeks after the parasitic infection with the pyrazole carbohydrazides for 45 days. Oral treatment with both compounds controlled evolution of footpad cutaneous lesions and dissemination of parasites to draining lymph nodes. Nitric oxide generation was observed in supernatants of lymph node cells from infected CBA mice that were treated with these compounds. The pyrazole carbohydrazide derivatives did not show any toxicity or cause alterations in body weight, plasma concentrations of alanine aminotransferase and aspartate aminotransferase, and urinary creatinine levels, but promoted a small decrease in blood neutrophils. These results provide new perspectives on the development of drugs with activities against leishmaniasis.

PMID: 19346377 [PubMed - in process]

10: Am J Trop Med Hyg. 2009 Apr;80(4):566-7.Click here to read

Evaluation of leishmanin skin test in Indian visceral leishmaniasis.

Gidwani K, Rai M, Chakravarty J, Boelaert M, Sundar S.

Department of Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.

We evaluated the performance of the leishmanin skin test (LST) in 50 patients with visceral leishmaniasis (VL), 124 cured VL patients at different time intervals, 125 healthy controls from an endemic region (HEC), and 14 healthy controls from a non-endemic region (NEHC). The leishmanin antigen used was based on Leishmania major and was obtained from the Pasteur Institute (Iran). A positive LST was found in 14.0% of patients with active VL, 40.3% of cured patients, 21.6% of HECs, and 0% in NEHCs. The 14% positivity in patients with active VL conflicts with the widely held opinion that such patients should be negative because of anergy. Also, a lack of sensitivity of the LST was observed in cured VL patients. An LST antigen produced from L. donovani strains from India should be explored.

PMID: 19346376 [PubMed - in process]

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