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Sent on Saturday, 2009 Mar 14Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
- 1: Acta Trop. 2009 Apr;110(1):80-5.
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Identification of genetic markers in sodium antimony gluconate (SAG) sensitive and resistant Indian clinical isolates of Leishmania donovani through amplified fragment length polymorphism (AFLP).
Division of Parasitology, Central Drug Research Institute, Lucknow, India.
Sodium Antimony Gluconate (SAG) is currently used worldwide as the first-line drugs for the treatment of visceral leishmaniasis (VL) and cutaneous leishmaniasis (CL) since 1940s. Unfortunately, the resistance of Leishmania parasite to this drug is increasing in several parts of the world. The mechanism of drug resistance in clinical isolates is still not very clear. Earlier, we have established a differentiation between six clinical isolates as sensitive and resistant on the basis of their sensitivity to SAG in vitro and in vivo as well as expression of proteophosphoglycan contents. In this preliminary study, we have further analyzed these isolates on the basis of their genetic diversity, molecular variance and phylogenetic structure using for the first time, a fingerprinting approach--amplified fragment length polymorphism (AFLP). Altogether 2338 informative AFLP bands were generated using 10 selective primer combinations. Percentage of polymorphism was 55.35%. A number of unique AFLP markers (217) were also identified in these strains. It was deduced that a higher rate of variations occurred among Leishmania clinical isolates which indicate the shifting of drug sensitive nature of parasite towards resistant condition.
PMID: 19283900 [PubMed - in process]
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- ReviewDrug resistance mechanisms in clinical isolates of Leishmania donovani. [Indian J Med Res. 2006]
- Epidemiological, clinical & pharmacological study of antimony-resistant visceral leishmaniasis in Bihar, India. [Indian J Med Res. 2004]
- Role of ABC transporter MRPA, gamma-glutamylcysteine synthetase and ornithine decarboxylase in natural antimony-resistant isolates of Leishmania donovani. [J Antimicrob Chemother. 2007]
- Evidence that the high incidence of treatment failures in Indian kala-azar is due to the emergence of antimony-resistant strains of Leishmania donovani. [J Infect Dis. 1999]
- Review[Treatment of visceral leishmaniasis in children] [Med Trop (Mars). 2007]
- 2: Scand J Immunol. 2009 Mar;69(3):251-8.
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An alkaloid extract of evanta, traditionally used as anti-leishmania agent in Bolivia, inhibits cellular proliferation and interferon-gamma production in polyclonally activated cells.
Department of Immunology, The Wenner Gren Institute, Stockholm University, Stockholm, Sweden. jaqueline.calla@imun.su.se
Traditional medicine and scientific studies have shown that the raw extract of Evanta [Galipea longiflora, Angostura longiflora (Krause) Kallunki] exhibits anti-leishmanial activity. We hypothesized that the healing observed when using this plant might not only be due to the direct action on the parasite, but possibly to a parallel effect on the host immune response to the parasite involved in the healing process. We show here that an alkaloid extract of Evanta (AEE) directly killed the parasite already at a dose of 10 microg/ml, but at this low concentration, AEE did not have a major effect on viability and proliferation of eukaryotic cells. The whole extract was also found to be stronger than 2-phenylquinoline, the most prominent alkaloid in AEE. AEE was not directly stimulating B or T cells or J774 macrophages. However, it interfered with the activation of both mouse and human T cells, as revealed by a reduction of in vitro cellular proliferation and interferon-gamma (IFN-gamma) production. The effect was more evident when the cells were pretreated with AEE and subsequently stimulated with the polyclonal T-cell activators Concanavalin A and anti-CD3. Taken together, our results suggest that Evanta have a direct leishmanicidal effect and due to the effect on IFN-gamma production it might contribute to control the chronic inflammatory reaction that characterize Leishmania infection pathology, but in vivo studies are necessary to corroborate this finding.
PMID: 19281537 [PubMed - in process]
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- Cellular and humoral immunity to Leishmania major in genetically susceptible mice after in vivo depletion of L3T4+ T cells. [J Immunol. 1987]
- Synergism between tumor necrosis factor-alpha and interferon-gamma on macrophage activation for the killing of intracellular Trypanosoma cruzi through a nitric oxide-dependent mechanism. [Eur J Immunol. 1992]
- Immune response in healthy volunteers vaccinated with killed leishmanial promastigotes plus BCG. I: Skin-test reactivity, T-cell proliferation and interferon-gamma production. [Vaccine. 1994]
- ReviewInterferon-gamma: biologic functions and HCV terapy (type I/II) (2 of 2 parts). [Clin Ter. 2006]
- ReviewReciprocal IFN-gamma and TGF-beta responses regulate the occurrence of mucosal inflammation. [Immunol Today. 1997]
- 3: J Parasitol. 2008 Dec;94(6):1428-9.
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First report of establishment of Trypanosoma evansi infection in pigeon nestlings (Columba livia).
Department of Beterinary Parasitology, Faculty of Veterinary and Animal Sciences, West Bengal University of Animal & Fishery Sciences, West Bengal, India.
Trypanosomosis (surra) caused by Trypanosoma evansi is quite common among horses where the parasite is endemic. In the present study, T. evansi was isolated from an infected horse and maintained by subinoculation in Swiss albino mice. At the peak of parasitemia (5 x 10(6) parasites per ml of blood), 0.25 ml of the tail blood from infected mice was inoculated intraperitoneally and subcutaneously to 2 groups of adult pigeons and 2 groups of pigeon nestlings. Four days after inoculation, the trypanosomes occurred in the peripheral circulation of pigeon nestlings, but no parasitemia was observed in adult pigeons. The body temperatures of infected nestlings increased to 104 F, whereas uninfected controls remained steady at 102 F; thus, elevated temperatures coincided with parasite presence in the peripheral circulation. A decrease in hemoglobin concentration of blood also was observed in infected nestlings. On microscopic examination, increases in length and breadth of trypomastigotes and vigorous flagellar movement of the parasites were observed. The virulence and pathogenicity of the parasites after adaptation to nestlings remained unchanged for albino mice as proved by the death of all subinoculated mice. Furthermore, polymerase chain reaction studies confirmed that the genomic DNA of trypanosomes in pigeon blood was the same as that of T. evansi. This is the first report of the establishment of T. evansi infection in pigeon nestlings.
PMID: 18576831 [PubMed - indexed for MEDLINE]
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Related Articles
- Comparative studies on the sensitivity of polymerase chain reaction and microscopic examination for the detection of Trypanosoma evansi in experimentally infected mice. [Comp Immunol Microbiol Infect Dis. 1998]
- Trypanosoma evansi: A comparison of PCR and parasitological diagnostic tests in experimentally infected mice. [Exp Parasitol. 2009]
- [Determination of the survival of Trypanosoma evansi in equine blood, using the microhematocrit method] [Rev Sci Tech. 1995]
- Endemic status of Trypanosoma evansi infection in a horse stable of eastern region of India--a field investigation. [Trop Anim Health Prod. 2008]
- ReviewTrypanosoma evansi and T. equiperdum: distribution, biology, treatment and phylogenetic relationship (a review). [Vet Parasitol. 1998]
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