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Sent on Saturday, 2010 Jun 26Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | Trop Anim Health Prod. 2010 Jun 26. [Epub ahead of print]Bovine trypanosomosis and its vectors in two districts of Bench Maji zone, South Western Ethiopia.Tadesse A, Tsegaye B.Department of Parasitology and Pathology, Faculty of Veterinary Medicine, Hawassa University, Hawassa, Ethiopia, abutadesse2@yahoo.com. AbstractA cross-sectional study was carried out from November 2008 to February 2009 in Guraferda and Sheko districts of Bench Maji Zone, South Western Ethiopia. The objective of the study was to determine the prevalence of bovine trypanosomosis and the density of its vectors. An overall prevalence of trypanosome infection in the study area was 4.4%. Trypanosoma congolense (36.36%) was the dominant trypanosome species followed by Trypanosoma vivax (18.18%) and Trypanosoma brucei (9.09%). Mean packed cell volume value of parasitemic animals (21.8%) was significantly (P < 0.05) lower than that of aparasitemic animals (27.7%). Biconical and NGU traps were deployed for 72 h, and the result indicated Glossina pallidipes followed by Glossina fuscipes as the only tsetse fly species caught in the study area along with other biting flies like Stomoxys and Tabanus. The apparent density of tsetse flies was 2.83 flies trap(-1) day(-1). NGU trap caught more of G. pallidipes while biconical trap caught more G. fuscipes, and the difference was significant (P < 0.05). Although the current study indicated low prevalence of trypanosomosis in the study area, the impacts of trypanosomosis on cattle production and productivity should not be neglected. Therefore, attention should be given to control the disease and also the vector. |
| PMID: 20577803 [PubMed - as supplied by publisher] | |
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| 2. | Biochim Biophys Acta. 2010 May 26. [Epub ahead of print]Regulatory role of nitric oxide in the reduced survival of erythrocytes in visceral leishmaniasis.Chowdhury KD , Sen G, Biswas T.Indian Institute of Chemical Biology, CSIR, Kolkata-700032, India. AbstractBACKGROUND: Nitric oxide (NO) plays a vital role in maintaining the survivability of circulating erythrocytes. Here we have investigated whether NO depletion associated with visceral leishmaniasis (VL) is responsible for the reduced survival of erythrocytes observed during the disease. METHODS: Infected hamsters were treated with standard anti-leishmanial sodium stibogluconate (SAG) and NO donor isosorbide dinitrate (ISD). Erythrophagocytosis by macrophages was determined by labelling the cells with FITC followed by flow cytometry. Aggregation of band3 was estimated from band3 associated EMA fluorescence. Caspase 3 activity was measured using immunosorbent assay kit. Phosphatidylserine (PS) externalization and cell shrinkage were determined using annexin V. Aminophspholipid translocase and scramblase activities were measured following NBD-PS and NBD-PC internalization, respectively. RESULTS: Impairment of both synthesis and uptake of NO resulted in decreased bioavailability of this signaling molecule in erythrocytes in VL. NO level was replenished after simultaneous treatment with ISD and SAG. Combination treatment decreased red cell apoptosis in infected animals by deactivating caspase 3 through s-nitrosylation. Drug treatment prevented infection-mediated ATP depletion and altered calcium homeostasis in erythrocytes. Improved metabolic environment effectively amended dysregulation of aminophospholipid translocase and scramblase, which in turn reduced cell shrinkage, and exposure of phosphatidylserine on the cell surface under the diseased condition. CONCLUSION AND GENERAL SIGNIFICANCE: In this study, we have identified NO depletion to be an important factor in promoting premature hemolysis with the progress of leishmanial infection. The study implicates NO to be a possible target for future drug development towards the promotion of erythrocyte survival in VL. Copyright © 2010. Published by Elsevier B.V. |
| PMID: 20576500 [PubMed - as supplied by publisher] | |
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| 3. | Immunobiology. 2010 Jun 4. [Epub ahead of print]Endothelial nitric oxide synthase limits the inflammatory response in mouse cutaneous leishmaniasis.Fritzsche C, Schleicher U, Bogdan C.Microbiology Institute-Clinical Microbiology, Immunology and Hygiene, University Hospital of Erlangen and Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany. AbstractEndothelial nitric oxide synthase (eNOS) was originally discovered in the cardiovascular system, where it contributes to the regulation of blood pressure and the inhibition of platelet adhesion. Considering that the vascular endothelium is critical for the initiation of inflammatory processes and that eNOS has been detected in certain types of immune cells, we investigated the function of eNOS in C57BL/6 mice infected with Leishmania major, a protozoan parasite that causes a chronic, but self-healing skin disease. C57BL/6 eNOS(-/-) mice developed more severe (but ultimately resolving) skin lesions with strikingly higher numbers of parasites compared to wildtype controls. In accordance with our finding that naive T lymphocytes and Th1 cells (as well as Th2 cells) did not express eNOS after stimulation and that eNOS was not required for Th1 differentiation in vitro, lymph node T cells from L. major-infected wildtype and eNOS(-/-) mice released comparable amounts of IFN-gamma and proliferated equally well. Immunohistological analyses revealed that the expression of inducible NO synthase in the skin and draining lymph nodes of infected mice was completely preserved in the absence of eNOS. However, the skin lesions of eNOS(-/-) mice were characterized by massive infiltrates of granulocytes, which in vitro similar to inflammatory macrophages failed to express eNOS. From these data, we conclude that during cutaneous leishmaniasis eNOS-derived NO, presumably released by vascular endothelial cells, counteracts the recruitment of granulocytes, which are known to function as host cells and trojan horses for Leishmania parasites, and thereby limits the severity of the skin lesions. Copyright © 2010. Published by Elsevier GmbH. |
| PMID: 20576313 [PubMed - as supplied by publisher] | |
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| 4. | BMC Microbiol. 2010 Jun 24;10(1):181. [Epub ahead of print]Comparison of BCG, MPL and cationic liposome adjuvant systems in leishmanial antigen vaccine formulations against murine visceral leishmaniasis.Ravindran R, Bhowmick S, Das A, Ali N.AbstractABSTRACT: BACKGROUND: The development of an effective vaccine against visceral leishmaniasis (VL) caused by Leishmania donovani is an essential aim for controlling the disease. Use of the right adjuvant is of fundamental importance in vaccine formulations for generation of effective cell-mediated immune response. Earlier we reported the protective efficacy of cationic liposome-associated L. donovani promastigote antigens (LAg) against experimental VL. The aim of the present study was to compare the effectiveness of two very promising adjuvants, Bacille Calmette-Guerin (BCG) and Monophosphoryl lipid A (MPL) plus trehalose dicorynomycolate (TDM) with cationic liposomes, in combination with LAg, to confer protection against murine VL. RESULTS: All the three formulations afforded significant protection against L. donovani in both the visceral organs, liver and spleen. Although comparable level of protection was observed in BCG+LAg and MPL-TDM+LAg immunized mice, highest level of protection was exhibited by the liposomal LAg immunized group. Significant increase in anti-LAg IgG levels were detected in both MPL-TDM+LAg and liposomal LAg immunized animals with higher levels of IgG2a than IgG1. But BCG+LAg failed to induce any antibody response. As an index of cell-mediated immunity DTH responses were measured and significant response was observed in mice vaccinated with all the three different formulations. However, highest responses were observed with liposomal vaccine immunization. Comparative evaluation of IFN-gamma and IL-4 responses in immunized mice revealed that MPL-TDM+LAg group produced the highest level of IFN-gamma but lowest IL-4 level, while BCG+LAg demonstrated generation of suboptimum levels of both IFN-gamma and IL-4 response. Elicitation of moderate levels of prechallenge IFN-gamma along with optimum IL-4 corresponds with successful vaccination with liposomal LAg. CONCLUSION: This comparative study reveals greater effectiveness of the liposomal vaccine for protection against progressive VL in BALB/c. Again, evaluation of the immune responses by vaccination emphasizes the need of stimulation of potent cellular immunity based on both Th1 and Th2 cell responses to confer protection against VL. |
| PMID: 20576102 [PubMed - as supplied by publisher] | |
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| 5. | Vector Borne Zoonotic Dis. 2010 Jun 24. [Epub ahead of print]Molecular Detection of Leishmania Infection Due to Leishmania major and Leishman ia turanica in the Vectors and Reservoir Host in Iran.Rassi Y, Oshaghi MA, Azani SM, Abaie MR, Rafizadeh S, Mohebai M, Mohtarami F, Zeinali MK.1 Department of Medical Entomology and Vector Control, School of Public Health, Tehran University of Medical Sciences , Tehran, Iran . AbstractAbstract An epidemiological study was carried out on the vectors and reservoirs of cutaneous leishmaniasis in rural areas of Damghan district, Semnan province, central Iran, during 2008-2009. Totally, 6110 sand flies were collected using sticky papers and were subjected to molecular methods for detection of Leishmania parasite. Phlebotomus papatasi Scopoli was the common species in outdoor and indoor resting places. Polymerase chain reaction technique showed that 24 out of 218 P. papatasi (11%) and 4 out of 62 Phlebotomus caucasicus Marzinovskyi (6.5%) were positive for parasites Leishmania major Yakimoff and Schokhor. Twenty-one rodent reservoir hosts captured using Sherman traps were identified as Rhombomys opimus Lichtenstein (95%) and Meriones libycus Lichtenstein (5%). Microscopic investigation on blood smear of the animals for amastigote parasites revealed 8 (40%) rodents infected with R. opimus. L. major infection in these animals was then confirmed by polymerase chain reaction against internal transcribed spacer ribosomal DNA (rDNA) loci of the parasite followed by restriction fragment length polymorphism. Further, sequence analysis of 297 bp of ITS1-rDNA loci revealed the presence of L. major and Leishmania turanica in P. papatasi, and L. major in R. opimus. This is the first molecular report of L. major infection in both vectors (P. papatasi and P. caucasicus) and reservoir host (R. opimus) in this region. The results indicated that P. papatas was the primary vector of the disease and circulating the parasite between human and reservoirs, and P. caucasicus could be considered as a secondary vector. Further, our study showed that R. opimus is the most important host reservoir for maintenance of the parasite source in the area. |
| PMID: 20575646 [PubMed - as supplied by publisher] | |
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| 6. | PLoS Pathog. 2010 Apr 29;6(4):e1000870.Impaired innate immunity in Tlr4(-/-) mice but preserved CD8+ T cell responses against Trypanosoma cruzi in Tlr4-, Tlr2-, Tlr9- or Myd88-deficient mice.Oliveira AC, de Alencar BC, Tzelepis F, Klezewsky W, da Silva RN, Neves FS, Cavalcanti GS, Boscardin S, Nunes MP, Santiago MF, Nóbrega A, Rodrigues MM, Bellio M.Instituto de Microbiologia Prof. Paulo de Góes, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, Rio de Janeiro, Brazil. AbstractThe murine model of T. cruzi infection has provided compelling evidence that development of host resistance against intracellular protozoans critically depends on the activation of members of the Toll-like receptor (TLR) family via the MyD88 adaptor molecule. However, the possibility that TLR/MyD88 signaling pathways also control the induction of immunoprotective CD8+ T cell-mediated effector functions has not been investigated to date. We addressed this question by measuring the frequencies of IFN-gamma secreting CD8+ T cells specific for H-2K(b)-restricted immunodominant peptides as well as the in vivo Ag-specific cytotoxic response in infected animals that are deficient either in TLR2, TLR4, TLR9 or MyD88 signaling pathways. Strikingly, we found that T. cruzi-infected Tlr2(-/-), Tlr4(-/-), Tlr9(-/) (-) or Myd88(-/-) mice generated both specific cytotoxic responses and IFN-gamma secreting CD8+ T cells at levels comparable to WT mice, although the frequency of IFN-gamma+CD4+ cells was diminished in infected Myd88(-/-) mice. We also analyzed the efficiency of TLR4-driven immune responses against T. cruzi using TLR4-deficient mice on the C57BL genetic background (B6 and B10). Our studies demonstrated that TLR4 signaling is required for optimal production of IFN-gamma, TNF-alpha and nitric oxide (NO) in the spleen of infected animals and, as a consequence, Tlr4(-/-) mice display higher parasitemia levels. Collectively, our results indicate that TLR4, as well as previously shown for TLR2, TLR9 and MyD88, contributes to the innate immune response and, consequently, resistance in the acute phase of infection, although each of these pathways is not individually essential for the generation of class I-restricted responses against T. cruzi. |
| PMID: 20442858 [PubMed - indexed for MEDLINE] | |
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