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 Saturday, 2010 Feb 27Search 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 |
| 1. | Int Arch Allergy Immunol. 2010 Feb 26;152(4):303-312. [Epub ahead of print]Dual Role of Interleukin-1alpha in Delayed-Type Hypersensitivity and Airway Hyperresponsiveness.Caucig P, Teschner D, Dinges S, Maxeiner JH, Reuter S, Finotto S, Taube C, von Stebut E.Department of Dermatology, Johannes Gutenberg University, Mainz, Germany. Background: Using a T helper (Th)1/Th2 disease model, we previously showed that genetically determined Th development depends on dendritic cell-derived interleukin (IL)-1alpha. In Leishmania major infections, Th1 immunity develops if IL-1alpha is present during T cell priming, whereas at later time points, IL-1alpha worsens disease outcome. In the present study, we determined the role of IL-1alpha in other Th2-mediated diseases. Methods: BALB/c mice were subjected to delayed-type hypersensitivity (DTH) or ovalbumin (OVA)/alum-induced allergic asthma in the presence or absence of IL-1alpha. Results: In DTH, mice treated with IL-1alpha during sensitization with keyhole limpet hemocyanin (KLH)/alum developed decreased footpad swelling associated with elevated KLH-specific interferon-gamma levels. In asthma, significantly decreased airway hypersensitivity responses (AHRs) were detected upon treatment with IL-1alpha during T cell priming. In contrast to control mice, IL-1alpha-treated mice showed reduced peribronchial inflammatory infiltrates. The bronchoalveolar lavage (BAL) fluid contained significantly decreased eosinophil numbers (approximately 50%), but 4 times more neutrophils. The BAL fluid of IL-1alpha-treated BALB/c exhibited reduced amounts of IL-5 and OVA-specific IgE serum levels. In contrast, IL-1alpha treatment at later time points after sensitization or during allergen challenge worsened AHR, had no effect on lung inflammation and BAL fluid cell composition. Furthermore, cytokine levels (IL-5, IL-13) and antigen-specific IgE were increased or unaltered under these conditions. Conclusion: Similarly to leishmaniasis, IL-1alpha administration during sensitization of Th2-mediated allergic reactions suppresses the course of disease by shifting the immune response towards Th1, whereas later treatments worsen disease outcome. Future studies will elucidate the therapeutic value of IL-1alpha in asthmatic patients. Copyright © 2010 S. Karger AG, Basel. |
| PMID: 20185922 [PubMed - as supplied by publisher] | |
| Related articles | |
| 2. | Lancet Infect Dis. 2010 Mar;10(3):184-194.Combination therapy for visceral leishmaniasis.van Griensven J, Balasegaram M, Meheus F, Alvar J, Lynen L, Boelaert M.Department of Clinical Sciences, Prince Leopold Institute of Tropical Medicine, Antwerp, Belgium. Combination therapy for the treatment of visceral leishmaniasis has increasingly been advocated as a way to increase treatment efficacy and tolerance, reduce treatment duration and cost, and limit the emergence of drug resistance. We reviewed the evidence and potential for combination therapy, and the criteria for the choice of drugs in such regimens. The first phase 2 results of combination regimens are promising, and have identified effective and safe regimens as short as 8 days. Several phase 3 trials are underway or planned in the Indian subcontinent and east Africa. The limited data available suggest that combination therapy is more cost-effective and reduces indirect costs for patients. Additional advantages are reduced treatment duration (8-17 days), with potentially better patient compliance and lesser burden on the health system. Only limited data are available on how best to prevent acquired resistance. Patients who are coinfected with visceral leishmaniasis and HIV could be a reservoir for development and spread of drug-resistant strains, calling for special precautions. The identification of a short, cheap, well-tolerated combination regimen that can be given in ambulatory care and needs minimal clinical monitoring will most likely have important public health implications. Effective monitoring systems and close regulations and policy will be needed to ensure effective implementation. Whether combination therapy could indeed help delay resistance, and how this is best achieved, will only be known in the long term. Copyright © 2010 Elsevier Ltd. All rights reserved. |
| PMID: 20185097 [PubMed - as supplied by publisher] | |
| Related articles | |
| 3. | Parasit Vectors. 2010 Feb 25;3(1):10. [Epub ahead of print]Natural infection of the sand fly Phlebotomus kazeruni by Trypanosoma species in Pakistan.Kato H, Uezato H, Sato H, Bhutto AM, Soomro FR, Baloch JH, Iwata H, Hashiguchi Y.ABSTRACT: The natural infection of phlebotomine sand flies by Leishmania parasites was surveyed in a desert area of Pakistan where cutaneous leishmaniasis is endemic. Out of 220 female sand flies dissected, one sand fly, Phlebotomus kazeruni, was positive for flagellates in the hindgut. Analyses of cytochrome b (cyt b), glycosomal glyceraldehyde phosphate dehydrogenase (gGAPDH) and small subunit ribosomal RNA (SSU rRNA) gene sequences identified the parasite as a Trypanosoma species of probably a reptile or amphibian. This is the first report of phlebotomine sand flies naturally infected with a Trypanosoma species in Pakistan. The possible infection of sand flies with Trypanosoma species should be taken into consideration in epidemiological studies of vector species in areas where leishmaniasis is endemic. |
| PMID: 20184773 [PubMed - as supplied by publisher] | |
| Related articles | |
| 4. | Nat Rev Immunol. 2010 Feb;10(2):80-1.Why does immunity to parasites take so long to develop?Yazdanbakhsh M, Sacks DL. |
| PMID: 20183893 [PubMed - indexed for MEDLINE] | |
| Related articles | |
MeSH Terms:
|
| 5. | Sci Signal. 2009 Nov 17;2(97):ra74.Trypanosoma cruzi targets Akt in host cells as an intracellular antiapoptotic strategy.Chuenkova MV, PereiraPerrin M.Parasitology Research Center, Department of Pathology, Tufts University School of Medicine, 150 Harrison Avenue, Boston, MA 02111, USA. The parasite Trypanosoma cruzi, which causes Chagas' disease, differentiates in the cytosol of its host cell and then replicates and spreads infection, processes that require the long-term survival of the infected cells. Here, we show that in the cytosol, parasite-derived neurotrophic factor (PDNF), a trans-sialidase that is located on the surface of T. cruzi, is both a substrate and an activator of the serine-threonine kinase Akt, an antiapoptotic molecule. PDNF increases the expression of the gene that encodes Akt while suppressing the transcription of genes that encode proapoptotic factors. Consequently, PDNF elicits a sustained functional response that protects host cells from apoptosis induced by oxidative stress and the proinflammatory cytokines tumor necrosis factor-alpha and transforming growth factor-beta. Given that PDNF also activates Akt by binding to the neurotrophic surface receptor TrkA, we propose that this protein activates survival signaling both at the cell surface, by acting as a receptor-binding ligand, and inside cells, by acting as a scaffolding adaptor protein downstream of the receptor. |
| PMID: 19920252 [PubMed - indexed for MEDLINE] | |
| Related articles | |
 | |
Publication Types:
MeSH Terms:
Substances:
Grant Support:
|
| 6. | Mem Inst Oswaldo Cruz. 2009 Aug;104(5):797-800.Performance levels of four Latin American laboratories for the serodiagnosis of Chagas disease in Mexican sera samples.Luquetti AO, Espinoza B, Martínez I, Hernández-Becerril N, Ponce C, Ponce E, Reyes PA, Hernández O, López R, Monteón V.Instituto de Patología Tropical e Saúde Pública, Universidade Federal de Goiás, Goiania, Brazil. In nearly all of the previous multicentre studies evaluating serological tests for Trypanosoma cruzi infection, sera samples from Central or South American countries have been used preferentially. In this work we compared the reliability of the serological tests using Mexican sera samples that were evaluated in four independent laboratories. This included a reference laboratory in Brazil and three participant laboratories, including one in Central America and two in Mexico. The kappa index between Brazilian and Honduran laboratories reached 1.0 and the index for the Mexican laboratories reached 0.94. Another finding of this study was that the source of antigen did not affect the performance of the serological tests. |
| PMID: 19820845 [PubMed - indexed for MEDLINE] | |
| Related articles Free article | |
 | |
Publication Types:
MeSH Terms:
Substances:
|
| 7. | Mem Inst Oswaldo Cruz. 2009 Aug;104(5):715-9.Epidermal growth factor receptors, testosterone levels and parotid gland changes in rats infected with Trypanosoma cruzi.Aguirre KL, Alves JB, Silva GA, Cardoso JE, Murta SM, Ferreira AJ.Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Av. Antônio Carlos 6627, Belo Horizonte, MG, Brazil. It has been demonstrated that parotid glands of rats infected with Trypanosoma cruzi present severe histological alterations; changes include reduction in density and volume of the acini and duct systems and an increase in connective tissue. We evaluated the association between morphological changes in parotid glands, circulating testosterone levels and epidermal growth factor receptor (EGF-R) expression in experimental Chagas disease in rats. Animals at 18 days of infection (acute phase) showed a significant decrease in body weight, serum testosterone levels and EGF-R expression in the parotid gland compared with a control group. Since decreases in body weight could lead to a reduction in circulating testosterone concentration, we believe that the reduction in EGF-R expression in parotid glands of infected rats is due to alterations in testosterone levels and atrophy of parotid glands is caused by changes in EGF-R expression. Additionally, at 50 days (chronic phase) of infection parotid glands showed a normal histological aspect likely due to the normalization of the body weight. These findings suggest that the testosterone-EGF-R axis is involved in the histological changes. |
| PMID: 19820831 [PubMed - indexed for MEDLINE] | |
| Related articles Free article | |
| | |
Publication Types:
MeSH Terms:
Substances:
|
| 8. | PLoS Negl Trop Dis. 2009 Jul 7;3(7):e488.Feasibility, drug safety, and effectiveness of etiological treatment programs for Chagas disease in Honduras, Guatemala, and Bolivia: 10-year experience of Médecins Sans Frontières.Yun O, Lima MA, Ellman T, Chambi W, Castillo S, Flevaud L, Roddy P, Parreño F, Albajar Viñas P, Palma PP.Médecins Sans Frontières/Doctors Without Borders, New York, New York, United States of America. BACKGROUND: Chagas disease (American trypanosomiasis) is a zoonotic or anthropozoonotic disease caused by the parasite Trypanosoma cruzi. Predominantly affecting populations in poor areas of Latin America, medical care for this neglected disease is often lacking. Médecins Sans Frontières/Doctors Without Borders (MSF) has provided diagnostic and treatment services for Chagas disease since 1999. This report describes 10 years of field experience in four MSF programs in Honduras, Guatemala, and Bolivia, focusing on feasibility protocols, safety of drug therapy, and treatment effectiveness. METHODOLOGY: From 1999 to 2008, MSF provided free diagnosis, etiological treatment, and follow-up care for patients <18 years of age seropositive for T. cruzi in Yoro, Honduras (1999-2002); Olopa, Guatemala (2003-2006); Entre Ríos, Bolivia (2002-2006); and Sucre, Bolivia (2005-2008). Essential program components guaranteeing feasibility of implementation were information, education, and communication (IEC) at the community and family level; vector control; health staff training; screening and diagnosis; treatment and compliance, including family-based strategies for early detection of adverse events; and logistics. Chagas disease diagnosis was confirmed by testing blood samples using two different diagnostic tests. T. cruzi-positive patients were treated with benznidazole as first-line treatment, with appropriate counseling, consent, and active participation from parents or guardians for daily administration of the drug, early detection of adverse events, and treatment withdrawal, when necessary. Weekly follow-up was conducted, with adverse events recorded to assess drug safety. Evaluations of serological conversion were carried out to measure treatment effectiveness. Vector control, entomological surveillance, and health education activities were carried out in all projects with close interaction with national and regional programs. RESULTS: Total numbers of children and adolescents tested for T. cruzi in Yoro, Olopa, Entre Ríos, and Sucre were 24,471, 8,927, 7,613, and 19,400, respectively. Of these, 232 (0.9%), 124 (1.4%), 1,475 (19.4%), and 1,145 (5.9%) patients, respectively, were diagnosed as seropositive. Patients were treated with benznidazole, and early findings of seroconversion varied widely between the Central and South American programs: 87.1% and 58.1% at 18 months post-treatment in Yoro and Olopa, respectively; 5.4% by up to 60 months in Entre Ríos; and 0% at an average of 18 months in Sucre. Benznidazole-related adverse events were observed in 50.2% and 50.8% of all patients treated in Yoro and Olopa, respectively, and 25.6% and 37.9% of patients in Entre Ríos and Sucre, respectively. Most adverse events were mild and manageable. No deaths occurred in the treatment population. CONCLUSIONS: These results demonstrate the feasibility of implementing Chagas disease diagnosis and treatment programs in resource-limited settings, including remote rural areas, while addressing the limitations associated with drug-related adverse events. The variability in apparent treatment effectiveness may reflect differences in patient and parasite populations, and illustrates the limitations of current treatments and measures of efficacy. New treatments with improved safety profiles, pediatric formulations of existing and new drugs, and a faster, reliable test of cure are all urgently needed. PMCID: PMC2700957 |
| PMID: 19582142 [PubMed - indexed for MEDLINE] | |
| Related articles Free article | |
  | |
Publication Types:
MeSH Terms:
Substances:
|
| 9. | PLoS Negl Trop Dis. 2009 Jul 7;3(7):e417.Differential regional immune response in Chagas disease.de Meis J, Morrot A, Farias-de-Oliveira DA, Villa-Verde DM, Savino W.Laboratory on Thymus Research, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil. jdemeis@ioc.fiocruz.br Following infection, lymphocytes expand exponentially and differentiate into effector cells to control infection and coordinate the multiple effector arms of the immune response. Soon after this expansion, the majority of antigen-specific lymphocytes die, thus keeping homeostasis, and a small pool of memory cells develops, providing long-term immunity to subsequent reinfection. The extent of infection and rate of pathogen clearance are thought to determine both the magnitude of cell expansion and the homeostatic contraction to a stable number of memory cells. This straight correlation between the kinetics of T cell response and the dynamics of lymphoid tissue cell numbers is a constant feature in acute infections yielded by pathogens that are cleared during the course of response. However, the regional dynamics of the immune response mounted against pathogens that are able to establish a persistent infection remain poorly understood. Herein we discuss the differential lymphocyte dynamics in distinct central and peripheral lymphoid organs following acute infection by Trypanosoma cruzi, the causative agent of Chagas disease. While the thymus and mesenteric lymph nodes undergo a severe atrophy with massive lymphocyte depletion, the spleen and subcutaneous lymph nodes expand due to T and B cell activation/proliferation. These events are regulated by cytokines, as well as parasite-derived moieties. In this regard, identifying the molecular mechanisms underlying regional lymphocyte dynamics secondary to T. cruzi infection may hopefully contribute to the design of novel immune intervention strategies to control pathology in this infection. PMCID: PMC2700264 |
| PMID: 19582140 [PubMed - indexed for MEDLINE] | |
| Related articles Free article | |
| | |
Publication Types:
MeSH Terms:
|
| 10. | PLoS Negl Trop Dis. 2009 Jun 2;3(6):e450.T. cruzi OligoC-TesT: a simplified and standardized polymerase chain reaction format for diagnosis of Chagas disease.Deborggraeve S, Coronado X, Solari A, Zulantay I, Apt W, Mertens P, Laurent T, Leclipteux T, Stessens T, Dujardin JC, Herdewijn P, Büscher P.Department of Parasitology, Institute of Tropical Medicine Antwerp, Antwerp, Belgium. sdeborggraeve@itg.be BACKGROUND: PCR has evolved into one of the most promising tools for T. cruzi detection in the diagnosis and control of Chagas disease. However, general use of the technique is hampered by its complexity and the lack of standardization. METHODOLOGY: We here present the development and phase I evaluation of the T. cruzi OligoC-TesT, a simple and standardized dipstick format for detection of PCR amplified T. cruzi DNA. The specificity and sensitivity of the assay were evaluated on blood samples from 60 Chagas non-endemic and 48 endemic control persons and on biological samples from 33 patients, 7 reservoir animals, and 14 vectors collected in Chile. PRINCIPAL FINDINGS: The lower detection limits of the T. cruzi OligoC-TesT were 1 pg and 1 to 10 fg of DNA from T. cruzi lineage I and II, respectively. The test showed a specificity of 100% (95% confidence interval [CI]: 96.6%-100%) on the control samples and a sensitivity of 93.9% (95% CI: 80.4%-98.3%), 100% (95% CI: 64.6%-100%), and 100% (95% CI: 78.5%-100%) on the human, rodent, and vector samples, respectively. CONCLUSIONS: The T. cruzi OligoC-TesT showed high sensitivity and specificity on a diverse panel of biological samples. The new tool is an important step towards simplified and standardized molecular diagnosis of Chagas disease. PMCID: PMC2685481 |
| PMID: 19503815 [PubMed - indexed for MEDLINE] | |
| Related articles Free article | |
| | |
Publication Types:
MeSH Terms:
Substances:
|
No comments:
Post a Comment