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Sent on Friday, 2011 Apr 29Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | PLoS Negl Trop Dis. 2011 Apr 19;5(4):e1042.Interferon-Gamma Release Assay (Modified QuantiFERON) as a Potential Marker of Infection for Leishmania donovani, a Proof of Concept Study.Gidwani K, Jones S, Kumar R, Boelaert M, Sundar S.SourceBanaras Hindu University, Varanasi, India. AbstractBACKGROUND:In areas endemic for visceral leishmaniasis (VL), a large number of infected individuals mount a protective cellular immune response and remain asymptomatic carriers. We propose an interferon-gamma release assay (IFN-γRA) as a novel marker for latent L. donovani infection. METHODS AND FINDINGS:We modified a commercial kit (QuantiFERON) evaluating five different leishmania-specific antigens; H2B, H2B-PSA2, H2B-Lepp12, crude soluble antigen (CSA) and soluble leishmania antigen (SLA) from L. donovani with the aim to detect the cell-mediated immune response in VL. We evaluated the assay on venous blood samples of active VL patients (n = 13), cured VL patients (n = 15), non-endemic healthy controls (n = 11) and healthy endemic controls (n = 19). The assay based on SLA had a sensitivity of 80% (95% CI = 54.81-92.95) and specificity of 100% (95% CI = 74.12-100). CONCLUSION:Our findings suggest that a whole-blood SLA-based QuantiFERON assay can be used to measure the cell-mediated immune response in L. donovani infection. The positive IFN-γ response to stimulation with leishmania antigen in patients with active VL was contradictory to the conventional finding of a non-proliferative antigen-specific response of peripheral blood mononuclear cells and needs further research. |
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| 2. | PLoS Negl Trop Dis. 2011 Apr 19;5(4):e1025.Isolation of Trypanosoma brucei gambiense from Cured and Relapsed Sleeping Sickness Patients and Adaptation to Laboratory Mice.Pyana PP, Ngay Lukusa I, Mumba Ngoyi D, Van Reet N, Kaiser M, Karhemere Bin Shamamba S, Büscher P.SourceInstitut National de Recherche Biomédicale, Kinshasa Gombe, Democratic Republic of the Congo. AbstractBACKGROUND:Sleeping sickness due to Trypanosoma brucei (T.b.) gambiense is still a major public health problem in some central African countries. Historically, relapse rates around 5% have been observed for treatment with melarsoprol, widely used to treat second stage patients. Later, relapse rates of up to 50% have been recorded in some isolated foci in Angola, Sudan, Uganda and Democratic Republic of the Congo (DRC). Previous investigations are not conclusive on whether decreased sensitivity to melarsoprol is responsible for these high relapse rates. Therefore we aimed to establish a parasite collection isolated from cured as well as from relapsed patients for downstream comparative drug sensitivity profiling. A major constraint for this type of investigation is that T.b. gambiense is particularly difficult to isolate and adapt to classical laboratory rodents. METHODOLOGY/PRINCIPAL FINDINGS:From 360 patients treated in Dipumba hospital, Mbuji-Mayi, D.R. Congo, blood and cerebrospinal fluid (CSF) was collected before treatment. From patients relapsing during the 24 months follow-up, the same specimens were collected. Specimens with confirmed parasite presence were frozen in liquid nitrogen in a mixture of Triladyl, egg yolk and phosphate buffered glucose solution. Isolation was achieved by inoculation of the cryopreserved specimens in Grammomys surdaster, Mastomys natalensis and SCID mice. Thus, 85 strains were isolated from blood and CSF of 55 patients. Isolation success was highest in Grammomys surdaster. Forty strains were adapted to mice. From 12 patients, matched strains were isolated before treatment and after relapse. All strains belong to T.b. gambiense type I. CONCLUSIONS AND SIGNIFICANCE:We established a unique collection of T.b. gambiense from cured and relapsed patients, isolated in the same disease focus and within a limited period. This collection is available for genotypic and phenotypic characterisation to investigate the mechanism behind abnormally high treatment failure rates in Mbuji-Mayi, D.R. Congo. |
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| 3. | J Res Med Sci. 2010 May;15(3):167-71.Soft tissue augmentation by autologous cultured fibroblasts transplantation for treatment of wrinkles and scars: a case series of 20 patients.Nilforoushzadeh MA, Siadat AH, Arianrad M, Moulavi F, Baradaran EH, Esfahani MH.SourceDermatologist, Associate Professor of Dermatology, Head of Skin Diseases and Leishmaniasis Research Center (Sedigheh Tahereh), Tehran University of Medical Sciences, Tehran, Iran. AbstractBACKGROUND:There are many filler agents for augmentation of static wrinkles and atrophic scars from synthetic, bio-synthetic, cadaver, animal and human sources. METHODS:The current study presents 20 patients whose facial wrinkles and lines were treated by transplantation of autologous cultured fibroblasts. The fibroblast nature of cells was confirmed by immune-staining and flow cytometry. RESULTS:The mean of improvement for this procedure at the 6 month follow up was 41%. CONCLUSIONS:In conclusion autologous fibroblast transplantation can be an effective procedure for correction of wrinkles and atrophic scars. |
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| 4. | J Res Med Sci. 2010 Mar;15(2):125-6.Treatment of atrophic cutaneous leishmaniasis scar using autologous fibroblasts and keratinocytes (a case report and literature review).Nilforoushzadeh MA, Esfahani MH, Fesharaki MA, Siadat AH, Ansari N, Baradaran EH.SourceDermatologist, Associated Professor of Dermatology, Head of Skin Diseases and Leishmaniasis Research Center (Sedigheh Tahereh), Isfahan University of Medical Sciences, Isfahan, Iran. |
| 5. | J Parasit Dis. 2010 Apr;34(1):1-13. Epub 2010 Oct 8.Drug targets in Leishmania.Chawla B, Madhubala R.SourceSchool of Life Sciences, Jawaharlal Nehru University, New Delhi, 110067 India. AbstractLeishmaniasis is a major public health problem and till date there are no effective vaccines available. The control strategy relies solely on chemotherapy of the infected people. However, the present repertoire of drugs is limited and increasing resistance towards them has posed a major concern. The first step in drug discovery is to identify a suitable drug target. The genome sequences of Leishmania major and Leishmania infantum has revealed immense amount of information and has given the opportunity to identify novel drug targets that are unique to these parasites. Utilization of this information in order to come up with a candidate drug molecule requires combining all the technology and using a multi-disciplinary approach, right from characterizing the target protein to high throughput screening of compounds. Leishmania belonging to the order kinetoplastidae emerges from the ancient eukaryotic lineages. They are quite diverse from their mammalian hosts and there are several cellular processes that we are getting to know of, which exist distinctly in these parasites. In this review, we discuss some of the metabolic pathways that are essential and could be used as potential drug targets in Leishmania. |
| 6. | J Invest Dermatol. 2011 Apr 28. [Epub ahead of print]A Role for Leukocyte-Derived IL-1RA in DC Homeostasis Revealed by Increased Susceptibility of IL-1RA-Deficient Mice to Cutaneous Leishmaniasis.Kautz-Neu K, Kostka SL, Dinges S, Iwakura Y, Udey MC, von Stebut E.SourceDepartment of Dermatology, Johannes-Gutenberg University, Mainz, Germany. AbstractDendritic cell (DC)-derived IL-1α/β plays a critical role in the induction of T helper type 1 (Th1)-dependent immunity against Leishmania. DCs from susceptible BALB/c mice produce less IL-1α/β when compared with resistant C57BL/6 mice, contributing to aberrant Th2 development and ultimate death of infected mice. We have extended our studies of the role of IL-1 in leishmaniasis using IL-1RA(-/-) BALB/c mice that are characterized by upregulated IL-1 receptor signaling. Unexpectedly, infection of IL-1RA(-/-) mice led to significantly worsened disease outcome with larger lesions, dramatically higher parasite burdens, and decreased IFN-γ production by antigen-specific T cells. We determined that IL-1RA(-/-) DCs were more mature already in the steady state, exhibited less phagocytotic capacity, and IL-12 production in response to various stimuli was impaired. Our data suggest that in addition to effects on Th education, IL-1α/β signaling also modulates DC homeostasis with increased signaling, leading to downmodulation of IL-12 synthesis and worsened disease outcome after infection with Leishmania major. Thus, the complex regulation of various members of the IL-1 cytokine family mediated through effects on both DCs and T cells critically contributes to disease outcome against this important human pathogen.Journal of Investigative Dermatology advance online publication, 28 April 2011; doi:10.1038/jid.2011.99. |
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| 7. | Autoimmun Rev. 2011 Jan;10(3):163-5. Epub 2010 Sep 29.Myocardial gene and protein expression profiles after autoimmune injury in Chagas' disease cardiomyopathy.Cunha-Neto E , Teixeira PC, Fonseca SG, Bilate AM, Kalil J.SourceLaboratory of Immunology, Heart Institute (InCor), University of São Paulo School of Medicine, São Paulo, Brazil. edecunha@usp.br AbstractOne third of the 16 million of individuals infected by the protozoan Trypanosoma cruzi in Latin America eventually develop chronic Chagas' disease cardiomyopathy (CCC), an inflammatory dilated cardiomyopathy with shorter survival than non-inflammatory cardiomyopathies. The presence of a T cell-rich mononuclear inflammatory infiltrate and the relative scarcity of parasites in the heart suggested that chronic inflammation secondary to the autoimmune recognition of cardiac proteins could be a major pathogenetic mechanism. Sera from CCC patients crossreactively recognize cardiac myosin and T. cruzi protein B13. T cell clones elicited from peripheral blood with T. cruzi B13 protein or its peptides could crossreactively recognize epitopes from cardiac myosin heavy chain. Likewise, CD4+ T cell clones infiltrating CCC myocardium crossreactively recognize cardiac myosin and T. cruzi protein B13, and intralesional T cell lines produce the inflammatory cytokines IFN-γ and TNF-α. Conversely, IFN-γ-induced genes and chemokines were found to be upregulated in CCC heart samples, and IFN-γ is able to induce cardiomyocyte expression of atrial natriuretic factor, a key member of the hypertrophy/heart failure signature. Proteomic analysis of CCC heart tissue showed reduced expression of the energy metabolism enzymes. It can be hypothesized that cytokine-induced modulation of cardiomyocyte gene/protein expression may be a novel disease mechanism in CCC, in addition to direct inflammatory damage. Copyright © 2010 Elsevier B.V. All rights reserved. |
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