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Sent on Thursday, 2010 Jan 07Search 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 One. 2010 Jan 5;5(1):e8468.Chaperone requirements for biosynthesis of the trypanosome variant surface glycoprotein.Field MC, Sergeenko T, Wang YN, Böhm S, Carrington M.Department of Pathology, University of Cambridge, Cambridge, United Kingdom. mcf34@cam.ac.uk BACKGROUND: Trypanosoma brucei does not respond transcriptionally to several endoplasmic reticulum (ER) stress conditions, including tunicamycin or dithiothreitol, indicating the absence of a conventional unfolded protein response. This suggests divergent mechanisms for quality control (QC) of ER protein folding and export may be present in trypanosomes. As the variant surface glycoprotein (VSG) represents approximately 90% of trypanosome plasma membrane protein, it is possible that VSG has evolved to fold efficiently to minimize ER folding burden. METHODOLOGY/PRINCIPAL FINDINGS: We demonstrate the presence of a QC system by pharmacological inhibition of the trypanosome 26S proteasome. This indicates active proteasome-mediated VSG turnover as approximately 2.5 fold more VSG is recovered from cell lysates following MG132 inhibition. An in silico scan of the trypanosome genome identified 28 open reading frames likely to encode polypeptides participating in ER nascent chain maturation. By RNA interference we monitored the importance of these gene products to proliferation, VSG abundance and cell morphology. 68% of the cohort were required for normal proliferation, and depletion of most of these factors resulted in increased VSG abundance, suggesting involvement in ERQC and degradation. CONCLUSIONS/SIGNIFICANCE: The retention of genes for, and the involvement of many gene products in, VSG folding indicates a substantial complexity within the pathways required to perform this role. Counterintuitively, for a super-abundant antigen VSG is apparently made in excess. The biosynthetic excess VSG appears to be turned over efficiently by the proteasome, implying that considerable VSG is rejected by the trypanosome ERQC mechanism. Accordingly, the VSG polypeptide is not well optimized for folding, as only approximately 30% attains the native state. Finally as much of the core ERQC system is functionally conserved in trypanosomes, the pathway has an ancient evolutionary origin, and was present in the last common eukaryotic ancestor. |
| PMID: 20052285 [PubMed - in process] | |
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| 2. | Can J Ophthalmol. 2009 Oct;44(5):47-48.Cutaneous leishmaniasis of the eyelid masquerading as basal cell carcinoma.Jaouni T, Deckel Y, Frenkel S, Ilsar M, Pe'er J. |
| PMID: 20052020 [PubMed - as supplied by publisher] | |
| 3. | J Clin Rheumatol. 2010 Jan;16(1):38-9.An atypical presentation of visceral leishmaniasis infection in a patient with rheumatoid arthritis treated with infliximab.Kritikos K, Haritatos E, Tsigkos S, Gounari P, Skrapari I, Gounaris T, Sioula E.1st Department of Internal Medicine, Evangelismos Hospital, Athens, Greece. konstantinoskritikos@yahoo.com Tumor necrosis factor alpha (TNF-alpha) is a cytokine, implicated in the pathogenesis of many inflammatory diseases, as well as in the immune-mediated response to infection, especially against intracellular pathogens. TNF-alpha antagonists have represented a revolution in the management of connective tissue diseases, such as rheumatoid arthritis. However, the use of these agents has been implicated with the emergence of a growing number of opportunistic infections. Here we report the case of a visceral Leishmaniasis in a 77-year-old woman who had been previously treated for rheumatoid arthritis with infliximab. The atypical presentation of this patient, previously treated with an anti-TNF-alpha biologic agent, where no splenomegaly or hepatomegaly was identified, is emphasized. |
| PMID: 20051756 [PubMed - in process] | |
| 4. | Public Health Genomics. 2009 Dec 29. [Epub ahead of print]Interleukin 10 Gene Polymorphisms and Development of Post Kala-Azar Dermal Leishmaniasis in a Selected Sudanese Population.Farouk S, Salih MA, Musa AM, Blackwell JM, Miller EN, Khalil EA, Elhassan AM, Ibrahim ME, Mohamed HS.Institute of Endemic Diseases, University of Khartoum, Khartoum, Sudan. Background: Post kala-azar dermal leishmaniasis (PKDL) is a cutaneous form of disease that develops at variable times after individuals have received treatment for clinical visceral leishmaniasis (VL). The study aimed to investigate the possible role of interleukin 10 (IL-10) and development of PKDL. Methods: 77 families composed of 41 complete case-parent trios and 36 case-parent pairs from the Masalit ethnic group were genotyped for 3 IL10 promoter polymorphisms: -1082A/G, -819C/T and -592C/A. Results: Single point analysis using the transmission disequilibrium test showed no evidence of association between any of these IL10 promoter single nucleotide polymorphisms (SNPs) and development of PKDL. Haplotype analysis performed using TRANSMIT showed borderline significance between PKDL and the haplotype AA across -592C/A and -1082A/G (p = 0.053). Haplotypes GCC (0.33) and ATA (0.30) were the common haplotypes in this Sudanese population. Allele frequencies for the 3 SNPs differed significantly in Sudan compared to other African (Gambian, Malawian, YRI) populations. Conclusion: There is no evidence for an association between 3 SNPs in the IL10 gene promoter and susceptibility to PKDL in the Masalit ethnic group in Sudan, although some evidence for haplotype association was observed. Copyright © 2009 S. Karger AG, Basel. |
| PMID: 20051670 [PubMed - as supplied by publisher] | |
| 5. | J Leukoc Biol. 2009 Nov;86(5):1239-46. Epub 2009 Jul 29.CCL2/MCP-1 controls parasite burden, cell infiltration, and mononuclear activation during acute Trypanosoma cruzi infection.Paiva CN, Figueiredo RT, Kroll-Palhares K, Silva AA, Silvério JC, Gibaldi D, Pyrrho Ados S, Benjamim CF, Lannes-Vieira J, Bozza MT.Departamento de Imunologia, Instituto de Microbiologia Prof Paulo de Góes, UFRJ, Av. Carlos Chagas Filho 373, CCS Bloco I, Ilha do Fundão, Rio de Janeiro, RJ, Brazil 21941-902. cnpaiva@iname.com CCL2/MCP-1 has emerged recently as a critical factor in infectious and autoimmune myocarditis. In fact, this chemokine is produced in great amounts in hearts from Trypanosoma cruzi-infected mice and is known to enhance parasite uptake and destruction by macrophages. Herein, we studied the involvement of CCL2 in tissue inflammation and resistance to T. cruzi. Infected CCL2(-/-) mice developed higher parasitemias and died earlier than WT mice. Close to their death, T. cruzi-infected CCL2(-/-) presented greater amounts of TNF, IFN-gamma, and IL-10 in plasma than WTs and clinical signs of systemic inflammatory response. Amastigote nests were more frequent in hearts and livers from infected CCL2(-/-) tissues than in WTs, and reduced numbers of leukocytes infiltrated their tissues. Leukocytes formed diffuse but not focal infiltrates in hearts from infected CCL2(-/-) mice, and perivascular cuffs could still be found in their livers. Infected CCL2(-/-) mice had smaller percentages of activated CD11b (Mac-1)+CD107b (Mac-3)+ macrophages and CD8+CD69(hi) cells among heart and liver infiltrates than WTs (flow cytometry), indicating that CCL2 controls subset migration/activation. CCL2 accumulated among focal heart infiltrates, suggesting that this chemokine is involved in retention of mononuclear cells in particular spots. Peritoneal macrophages from CCL2(-/-) mice displayed decreased trypanocidal activity. Our results demonstrate that CCL2 contributes to reduce parasite growth and indicate that it does so by controlling the distribution, cellular composition, and state of activation of inflammatory infiltrates in acute T. cruzi infection. |
| PMID: 19641038 [PubMed - indexed for MEDLINE] | |
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