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Sent on Friday, 2010 Jan 22Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| 1. | Indian J Pathol Microbiol. 2010 Jan-Mar;53(1):172-3.Cutaneous leishmaniasis in a soldier.Moiz B, Beg MA, Ali N.Department of Pathology & Microbiology, The Aga Khan University, Karachi, Pakistan. |
| PMID: 20090261 [PubMed - in process] | |
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| 2. | Indian J Pathol Microbiol. 2010 Jan-Mar;53(1):96-100.Morphological findings in bone marrow biopsy and aspirate smears of visceral kala azar: A review.Dhingra KK, Gupta P, Saroha V, Setia N, Khurana N, Singh T.Department of Pathology, Maulana Azad Medical College and Lok Nayak Hospital, Bahadur Shah Zafar Marg, New Delhi - 110 002, India. Context: Visceral leishmaniasis (VL) is endemic in India and may simulate and cause many hematological disorders like pancytopenia, myelofibrosis, myelodysplasia and hemophagocytosis. Aims: The study aims to investigate the hematological manifestation of Visceral Leishmaniasis and associated changes that may be observed in bone marrow aspirate smears and biopsy which may warn a pathologist of possible infections. Settings and Design: This is a retrospective study of 18 VL cases on B (b) one marrow aspirate and biopsy in the department of Pathology in a tertiary care teaching hospital in New Delhi. Methods and Material: Giemsa stained slides of bone marrow aspirates and hematoxylin and Eosin stained biopsy slides were reviewed in detail by two competent pathologists. All the findings were tabulated and discussed and comparisons made with the previous similar studies. Results: Hyper cellular marrow, increased lymphocytes and plasma cells, marrow granulomas, hemophagocytosis, myelofibrosis, myelodysplasia and gelatinous transformation of the marrow were notable features the presence of which together or individually should caution a pathologist to search for Leishman Donovan (LD) bodies in patients especially in a non-endemic zone in a tropical country. |
| PMID: 20090232 [PubMed - in process] | |
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| 3. | J Immunol. 2010 Jan 20. [Epub ahead of print]Invariant NKT Cells Preferentially Modulate the Function of CD8{alpha}+ Dendritic Cell Subset in Inducing Type 1 Immunity against Infection.Joyee AG, Uzonna J, Yang X.Department of Medical Microbiology and. Although studies suggest that NKT cell (NKT) activation modulates the function of dendritic cells (DCs) in inducing T cell responses, it is unknown whether this modulating effect is biased to a DC subset. We previously reported that NKT activation could modulate DC function in inducing protective T cell immunity to Chlamydia pneumoniae, an intracellular bacterial infection. In this study, we investigated the effect of NKT activation on DC subsets, using multiple approaches, including gene knockout mice, alpha- galactosylceramide stimulation, adoptive transfer of invariant NKT (iNKT), and functional analysis of DC subsets in both in vitro and in vivo settings. We found a preferential modulating effect of iNKTs on the CD8alpha(+) DC subset. Specifically, we found that iNKT-deficient mice, compared with wild-type (WT) mice, showed reduced CD8alpha(+) DC expansion with lower CD40 expression and IL-12 production, whereas enhancing iNKT activation in WT mice or adoptive transfer of iNKTs to Jalpha18(-/-) mice resulted in increased function of CD8alpha(+) DCs in inducing type 1 immune responses. Further, DC-iNKT coculture experiments showed a direct CD40L-dependent enhancing effect of iNKTs on IL-12p70 production by CD8alpha(+) DCs. More importantly, CD8alpha(+) DCs from Jalpha18(-/-) mice, compared with those from WT mice, showed significantly reduced ability to activate IFN-gamma-producing T cells in vitro and to induce type 1 immunity and protection in vivo. Moreover, a similar CD8alpha(+) DC subset alteration was found in the Jalpha18(-/-) mice following Leishmania major infection. Our data provide the first direct evidence that iNKTs preferentially promote the functional development of a subset of DC to generate protective immunity against infections. |
| PMID: 20089704 [PubMed - as supplied by publisher] | |
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| 4. | J Antimicrob Chemother. 2010 Jan 20. [Epub ahead of print]In vitro activity of anti-leishmanial drugs against Leishmania donovani is host cell dependent.Seifert K, Escobar P, Croft SL.London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK. Objectives To evaluate the in vitro activity of anti-leishmanial drugs against intracellular Leishmania donovani amastigotes in different types of macrophages. Methods Mouse peritoneal macrophages (PEMs), mouse bone marrow-derived macrophages (BMMPhi), human peripheral blood monocyte-derived macrophages (PBMPhi) and differentiated THP-1 cells were infected with L. donovani. Cultures were incubated with sodium stibogluconate, amphotericin B deoxycholate (Fungizone((R))), miltefosine or paromomycin sulphate over six concentrations in 3-fold serial dilutions for 5 days. Analysis was based on percentage inhibition of infected macrophages and EC(50)/EC(90) values estimated using sigmoidal curve-fitting. Results The rank order of drug activity was the same in the different macrophage populations: amphotericin B > miltefosine > sodium stibogluconate > paromomycin. However, significant (P < 0.05) differences were observed between populations. Amphotericin B was more active in PEMs and BMMPhi (EC(50) 0.02-0.06 microM) compared with PBMPhi and differentiated THP-1 cells (EC(50) 0.08-0.40 microM) and miltefosine was more active in PBMPhi (EC(50) 0.16-0.74 microM) compared with PEMs and BMMPhi (EC(50) 2.60-7.67 microM). Sodium stibogluconate displayed highest activity in PBMPhi (EC(50) 1.38-1.89 microg Sb(v)/mL), followed by PEMs (EC(50) 21.75-27.79 microg Sb(v)/mL) and BMMPhi and differentiated THP-1 cells (EC(50) 28.96-112.77 microg Sb(v)/mL). Paromomycin showed highest activity in PBMPhi (EC(50) 80.03-104.38 microM) and PEMs (EC(50) 75.42-201.63 microM). Conclusions In vitro activity of anti-leishmanial drugs is host cell dependent. This has implications for: (i) the evaluation of in vitro drug activity; (ii) the evaluation of drug susceptibility of clinical isolates; and (iii) the standardization of anti-leishmanial drug assays. |
| PMID: 20089542 [PubMed - as supplied by publisher] | |
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| 5. | Int J Health Geogr. 2010 Jan 21;9(1):2. [Epub ahead of print]Ecological niche model of Phlebotomus alexandri and P. papatasi (Diptera: Psychodidae) in the Middle East.Colacicco-Mayhugh MG, Masuoka PM, Grieco JP.ABSTRACT: BACKGROUND: The purpose of this study is to create distribution models of two sand fly species, Phlebotomus papatasi (Scopoli) and P. alexandri (Sinton), across the Middle East. Phlebotomus alexandri is a vector of visceral leishmaniasis, while P. papatasi is a vector of cutaneous leishmaniasis and sand fly fever. Collection records were obtained from literature reports from 1950 through 2007 and unpublished field collection records. Environmental layers considered in the model were elevation, precipitation, land cover, and WorldClim bioclimatic variables. Models were evaluated using the threshold-independent area under the curve (AUC) receiver operating characteristic analysis and the threshold-dependent minimum training presence. RESULTS: For both species, land cover was the most influential environmental layer in model development. The bioclimatic and altitude variables all contributed to model development; however, none influenced the model as strongly as land cover. CONCLUSION: While not perfect representations of the absolute distribution of P. papatasi and P. alexandri, these models indicate areas with a higher probability of presence of these species. This information could be used to help guide future research efforts into the ecology of these species and epidemiology of the pathogens that they transmit. |
| PMID: 20089198 [PubMed - as supplied by publisher] | |
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| 6. | BMC Med Genet. 2010 Jan 20;11(1):10. [Epub ahead of print]CXCR1 and SLC11A1 polymorphisms affect susceptibility to cutaneous leishmaniasis in Brazil: a case-control and family-based study.Castellucci L, Jamieson SE, Miller EN, Menezes E, Oliveira J, Magalhaes A, Guimaraes LH, Lessa M, Ribeiro de Jesus A, Carvalho EM, Blackwell JM.ABSTRACT: BACKGROUND: L. braziliensis causes cutaneous (CL) and mucosal (ML) leishmaniasis. Wound healing neutrophil (PMN) and macrophage responses made following the bite of the vector sand fly contribute to disease progression in mice. To look at the interplay between PMN and macrophages in disease progression in humans we asked whether polymorphisms at genes that regulate their infiltration or function are associated with different clinical phenotypes. Specifically, CXCR1 (IL8RA) and CXCR2 (IL8RB) are receptors for chemokines that attract PMN to inflammatory sites. They lie 30-260 kb upstream of SLC11A1, a gene known primarily for its role in regulating macrophage activation, resistance to leishmaniasis, and wound healing responses in mice, but also known to be expressed in PMN, macrophages and dendritic cells. METHODS: Polymorphic variants at CXCR1, CXCR2 and SLC11A1 were analysed using Taqman or ABI fragment separation technologies in cases (60 CL; 60 ML), unrelated controls (n=120), and multicase families (104 nuclear families; 88 ML, 250 CL cases) from Brazil. Logistic regression analysis, family-based association testing (FBAT) and haplotype analysis (TRANSMIT) were performed. RESULTS: Case-control analysis showed association between the common C allele (OR 2.38; 95% CI 1.23-4.57; P=0.009) of CXCR1_rs2854386 and CL, supported by family-based (FBAT; Z score 2.002; P=0.045) analysis (104 nuclear families; 88 ML, 250 CL cases). ML associated with the rarer G allele (Z score 1.999; P=0.046). CL associated with a 3' insertion/deletion polymorphism at SLC11A1 (Z score 2.549; P=0.011). CONCLUSIONS: The study supports roles for CXCR1 and SLC11A1 in the outcome of L. braziliensis infection in humans. Slc11a1 does not influence cutaneous lesion development following needle injection of Leishmania in mice, suggesting that its role here might relate to the action of PMN, macrophage and/or dendritic cells in the wound healing response to the sand fly bite. Together with the CXCR1 association, the data are consistent with hypotheses relating to the possible role of PMN in initiation of a lesion following the delivery of parasites via the sand fly bite. Association of ML with the rare derived G allele suggests that PMN also have an important positive role to play in preventing this form of the disease. |
| PMID: 20089160 [PubMed - as supplied by publisher] | |
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| 7. | Cell Microbiol. 2010 Jan 20. [Epub ahead of print]Proteophosphoglycan confers resistance of Leishmania major to midgut digestive enzymes induced by blood feeding in vector sand flies.Secundino N, Kimblin N, Peters NC, Lawyer P, Capul AA, Beverley SM, Turco SJ, Sacks D.Laboratory of Parasitic Diseases, NIAID, NIH, Bethesda MD, 20892. Summary Leishmania synthesize abundant phosphoglycan-containing molecules made up of [Gal-Man-PO4] repeating units, including the surface lipophosphoglycan (LPG), and the surface and secreted proteophosphoglycan (PPG). The vector competence of Phlebotomusduboscqi and Lutzomyia longipalpis sand flies was tested using L. major knockout mutants deficient in either total phosphoglycans (lpg2(- )or lpg5A(-)/5B(-)) or LPG alone (lpg1(-)) along with their respective gene add back controls. Our results confirm that LPG, the major cell surface molecule of Leishmania promastigotes known to mediate attachment to the vector midgut, is necessary to prevent the loss of infection during excretion of the blood meal remnants from a natural vector, P. duboscqi, but not an unnatural vector, L. longipalpis. Midgut digestive enzymes induced by blood feeding pose another potential barrier to parasite survival. Our results show that 36-72 hours after the infective feed, all parasites developed well except the lpg2(-) and lpg5A(-)/5B(-) mutants which showed significantly reduced survival and growth. Protease inhibitors promoted the early survival and growth of lpg2(-) in the blood meal. PPG was shown to be the key molecule conferring resistance to midgut digestive enzymes, as it prevented killing of lpg2(-) promastigotes exposed to midgut lysates prepared from blood-fed flies. The protection was not associated with inhibition of enzyme activities, but with cell surface acquisition of the PPG, which appears to function similar to mammalian mucins to protect the surface of developing promastigotes against proteolytic damage. |
| PMID: 20088949 [PubMed - as supplied by publisher] | |
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| 8. | Infect Immun. 2010 Jan;78(1):231-40. Epub 2009 Oct 19.Localization and developmental regulation of a dispersed gen e family 1 protein in Trypanosoma cruzi.Lander N, Bernal C, Diez N, Añez N, Docampo R, Ramírez JL.Centro de Biotecnología, Instituto de Estudios Avanzados, Caracas 1080, Venezuela. The dispersed gene family 1 (DGF-1) is the fifth largest gene family in the Trypanosoma cruzi genome, with over 500 members (11). Many of the predicted DGF-1 protein products have several transmembrane domains and N-glycosylation and phosphorylation sites and were thought to localize in the plasma membrane. Here, we report that affinity-purified antibodies against a region of one of these proteins (DGF-1.2) localized it intracellularly in different stages of the parasite. DGF-1.2 is more abundant in the amastigote stage than in trypomastigotes and epimastigotes, as detected by immunofluorescence and Western blot analyses. The protein changed localization during intracellular or extracellular differentiation from the trypomastigote to the amastigote stage, where it finally localized to small bodies in close contact with the inner side of the amastigote plasma membrane. DGF-1.2 did not colocalize with markers of other subcellular organelles, such as acidocalcisomes, glycosomes, reservosomes, lipid droplets, or endocytic vesicles. During extracellular differentiation, the protein was detected in the culture medium from 0 to 22 h, peaking at 14 h. The presence of DGF-1.2 in the differentiation culture medium was confirmed by mass spectrometry analysis. Finally, when epimastigotes were subjected to starvation, there was a decrease in the labeling of the cells and, in Western blots, the appearance of bands of lower molecular mass, suggesting its cleavage. These results represent the first report of direct immunodetection and developmental expression and secretion of a DGF-1 protein. PMCID: PMC2798230 [Available on 2010/7/1] |
| PMID: 19841080 [PubMed - indexed for MEDLINE] | |
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| 9. | Ann Trop Med Parasitol. 2009 Sep;103(6):471-6.Aetiological treatment with itraconazole or ketoconazole in individuals with Trypanosoma cruzi/HIV co-infection.de Almeida EA, Silva EL, Guariento ME, Aoki FH, Pedro Rde J.Department of Internal Medicine, Faculty of Medical Science, University of Campinas - UNICAMP, SP, Brazil. eros@fcm.unicamp.br Two Brazilian cases of Trypanosoma cruzi/HIV co-infection have recently been treated with azole derivatives. Benznidazole, the drug generally used for the treatment of Chagas disease, was initially used in one case but discontinued because of an adverse effect (retrobulbar neuritis) and replaced by itraconazole. The other case had oesophageal candidiasis, which was treated with ketoconazole, a drug that had already been shown to be effective in the treatment of Chagas disease. Since the medications were effective in reducing the T. cruzi parasitaemia in both patients, they probably helped prevent the severe morbidity sometimes associated with Chagas disease, although the HIV infections still proved fatal in both cases. |
| PMID: 19695152 [PubMed - indexed for MEDLINE] | |
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| 10. | Biol Lett. 2009 Dec 23;5(6):798-801. Epub 2009 Jul 15.A distinct infection cost associated with trans-generational priming of antibacterial immunity in bumble-bees.Sadd BM, Schmid-Hempel P.Institute of Integrative Biology, ETH Zurich, Universitätstrasse 16, 8092 Zürich, Switzerland. ben.sadd@env.ethz.ch The adaptive value of facultative maternal adjustment of offspring immunity, or trans-generational immune-priming, will depend on the ecological background. In particular, where there is a mismatch between the immune adjustment and offspring environment, the immunological link between mothers and offspring may be disadvantageous owing to the presence of associated costs. Costs to an individual of responding to an immune challenge are extensively documented. However, in addition to parents, the relevant costs for trans-generational immune-priming also pertain to offspring, but as yet it is unknown what costs offspring will bear. In bumble-bees, higher antibacterial activity has been shown as a trans-generational effect when mothers receive a bacterial-based immune challenge prior to colony founding. Here we show that while naive offspring from immune-challenged mothers do not show evidence for a direct energy-related survival cost, they do show increased susceptibility to a parasite distinctly unrelated to the maternal challenge. The presence of costs associated with trans-generational immune-priming will shape the evolution of this trait depending on the ecological setting. |
| PMID: 19605389 [PubMed - indexed for MEDLINE] | |
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