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Sent on Wednesday, 2011 Nov 30Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| 1. | Eur J Immunol. 2011 Dec;41(12):3396-400. doi: 10.1002/eji.201190075.Immunological consequences of arthropod vector-derived salivary factors.Leitner WW, Costero-Saint Denis A, Wali T.SourceDivision of Allergy, Immunology and Transplantation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. wleitner@niaid.nih.gov. AbstractDiseases, such as malaria, dengue, leishmaniasis and tick-borne encephalitis, affect a substantial percentage of the world's population and continue to result in significant morbidity and mortality. One common aspect of these diseases is that the pathogens that cause them are transmitted by the bite of an infected arthropod (e.g. mosquito, sand fly, tick). The pathogens are delivered into the skin of the mammalian host along with arthropod saliva, which contains a wide variety of bioactive molecules. These saliva components are capable of altering hemostasis and immune responses and may contribute to the ability of the pathogen to establish an infection. The biological and immunological events that occur during pathogen transmission are poorly understood but may hold the key to novel approaches to prevent transmission and/or infection. In May 2011, the National Institute of Allergy and Infectious Diseases (NIAID) of the US National Institutes of Health (NIH) in the Department of Health and Human Services hosted a workshop entitled Immunological Consequences of Vector-Derived Factors which brought together experts in skin immunology, parasitology and vector biology to outline the gaps in our understanding of the process of pathogen transmission, to explore new approaches to control pathogen transmission, and to initiate and foster multidisciplinary collaborations among these investigators. Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. |
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| 2. | Eur J Immunol. 2011 Dec;41(12):3388-9. doi: 10.1002/eji.201190071.In this issue.[No authors listed]AbstractCOVER IMAGE: The cover image shows immunohistological analysis of a spleen section from QMxB6 mice 96 hours after immunization with NP-Ficoll. IgD staining (brown) de termines the B-cell follicles and NP-staining (blue) the antibody-producing cells; plasmablasts (dark blue regions) are present in the red pulp, and germinal centres (pale blue) can be seen in the follicles; the T zones (which lack B cells) remain unstained. The image is kindly provided by Jennifer Marshall and relates to the study Marshall et al. (pp. 3506-3512) in which it is shown that Ig class-switch recombination during extrafollicular responses occurs at the B blast rather than the plasmablast stage. INKT CELLS IN DIABETES: THE GOOD, THE BAD AND THE BALANCE: Invariant natural killer T (iNKT) cells are innate-like T lymphocytes highly conserved in mice and humans. Type 1 diabetes (T1D) is an autoimmune disease caused by the destruction of insulin-producing pancreatic beta cells. Studies in mouse models have demonstrated the protective role of iNKT cells in the development of T1D. Recently, a new subset of iNKT cells producing high levels of the pro-inflammatory cytokine IL-17 has been identified (iNKT17). In this issue, Simoni et al. show that the non-obese diabetic (NOD) mouse, which spontaneously develops T1D, exhibits a larger iNKT17 cell population as compared with non-autoimmune C57BL/6 mice. iNKT17 cells infiltrating the pancreas of NOD mice are locally activated and produce IL-17. Contrary to the protective role of CD4(+) iNKT cells, CD4(-) iNKT cells, containing an iNKT17 cell population, exacerbate diabetes in an IL-17-dependent manner. Therefore, the balance between protective and deleterious iNKT cells is a key parameter controlling autoimmunity. pp. 3574-3585 VACCINE VECTOR TYPES AND COMBINATIONS DETERMINE T-CELL QUALITY: Different pathogens stimulate different innate responses, which in turn lead to distinct qualities of the elicited T cells. T-cell quality plays a key role in orchestrating immune responses and delivering the ultimate effector control of invaders. By the same token, different vaccine modalities employing the same transgenic antigen induce different qualities of transgene-specific T cells. Therefore, vaccines using benign viruses and bacteria as vectors are predisposed to prime T cells that control some pathogens better than others. Furthermore, vaccine combinations in heterologous prime-boost regimens not only enhance transgene-specific T-cell frequency, but allow for tuning of effector and memory T-cell qualities. In this issue, Hopkins et al. map the unique signatures of intercellular signaling molecules released by T cells elicited by six different HIV-1 vaccine candidates used singularly and in combination in mice. A truly rational vaccine regimen design awaits a more complete understanding of the workings of the immune system and its interactions with HIV-1. pp. 3542-3552 TH1- AND TH2-INDUCING DC PROFILES REVEAL QUANTITATIVE DIFFERENCES IN MATURATION: The maturation or activation of dendritic cells (DCs) is required to ignite efficient T-cell responses. The differences in the nature of pathogens with various pathogen-associated molecular patterns (PAMPs) have been proposed to direct either the Th1 or Th2 polarization of CD4(+) T cells. In addition, inflammatory or infectious signaling pathways would be expected to raise different qualities of matured DCs. In this issue, Pletinckx et al. show that the maturation signatures and functionality of DCs matured by inflammatory signals (TNF) or pathogen-derived signals (Th2-inducing Trypanosoma brucei antigens) in mice are highly similar. Strikingly, the difference in regulated genes between the Th2-inducing DCs (160-466 genes) and LPS-matured Th1-inducing DCs (4969 genes) are mainly quantitative. Repetitive Th2 induction further shifts DC maturation to IL-10(+) Tr1-like cells. Thus, the data indicate that simply the strength of DC maturation may dictate Th1/Th2 polarization. pp. 3479-3494 HOW PALMITOYLATION MODULATES THE IMMUNE SYSTEM: The human NKG2D receptor activates the immune response in lymphocytes, including CD8(+) T cells and natural killer cells. In cells undergoing stress, such as transformation and viral infection, the expression of NKG2D ligands is induced. While binding of ligand to NKG2D triggers cytokine secretion and/or cytotoxicity, release of soluble ligand into the milieu downmodulates the receptor function of NKG2D. In this issue, Agüera-González et al. explore the role of a post-translational modification of the NKG2D ligand MICA on its expression and functional consequences. Two cysteine residues in MICA are identified whose mutation impedes palmitoylation of MICA. Recruitment of MICA to membrane microdomains of CHO cells, where it encounters the metalloprotease responsible for its shedding, is shown to be palmitoylation-dependent. Nonpalmitoylated MICA is released inefficiently from cells, whereas target CHO cells expressing the mutant MICA are recognized by NKG2D for cytotoxicity. These data indicate that post-translational modification of MICA differentially regulates protein shedding and immune recognition. pp. 3667-3676 DOES NOD2 HAVE ANY T-CELL INTRINSIC ROLE?: Nod2 is a member of the family of cytosolic innate immune receptors called Nod-like receptors, and recognizes bacterial cell wall components. Mutations in the Nod2 gene are highly associated with an elevated risk of Crohn's disease. A recent article reported that Nod2 has a T-cell intrinsic role, and is important for the induction of Th1 immune responses and protection against Toxoplasma gondii infection. In this issue Caetano et al. show, in a collaborative work repeated in three independent laboratories, that Nod2 is not important for host defense against T. gondii. Nod2-deficient mice are fully capable of inducing Th1 immune responses and do not show enhanced susceptibility to T. gondii infection. Upon TCR stimulation in vitro, Nod2-deficient CD4(+) T cells show normal activation, IL-2 production, proliferation and Th1/Th2 differentiation. These data strongly support the idea that Nod2 does not play any role in T-cell differentiation to Th1 and Th2 subsets. pp. 3627-3631. Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. |
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| 3. | Rev Bras Reumatol. 2011 Dec;51(6):579-586.Anti-citrullinated peptide antibodies and rheumatoid factor in Sudanese patients with Leishmania donovani infection. [Article in English, Portuguese] Ahlin E, Elshafei A, Nur M, El Safi SH, Johan R, Elghazali G.SourceUnidade de Imunologia Clínica, Uppsala University, Uppsala, Suécia. AbstractOBJECTIVE:The present study evaluated the presence of anti-cyclic citrullinated peptides antibodies (anti-CCP), rheumatoid factor (RF), and circulating immune complexes (CIC) in Sudanese patients infected with the Leishmania donovani parasite. PATIENTS AND METHODS:Sera were collected from Leishmania infected patients (n = 116) and healthy Sudanese (n = 93). Nineteen Sudanese anti-CCP+ RA patients were included as positive controls. Levels of CIC and anti-CCP were measured by ELISA. Control plate with cyclic control peptides containing arginine instead of citrulline was used to evaluate citrulline specifi c reactivity. RESULTS:Among Leishmania-infected patients and anti-CCP+ RA patients, most were RF positive (86%), while the frequency of CIC positivity was higher among visceral leishmaniasis (VL) patients (VL 38%; anti-CCP+ RA 24%). When anti-CCP reactivity was analysed, 12% of VL patients were found to be positive. The levels of anti-CCP among VL patients correlated well with the CIC levels found (r = 0.65, P < 0.0001). In RA group, no association was found between CIC and anti-CCP. The possibility that anti-CCP positivity was due to cross reactions with CIC was experimentally ruled out. Contrary to what was seen in Sudanese RA sera, the CCP reactivity was not restricted to citrulline but reacted equally well with the arginine control peptide. CONCLUSION:The finding that CCP reactivity was not restricted to citrulline argues that this is more an effect of extensive inflammation and immune activation than a sign of shared pathogenic characteristics with anti-CCP arthritis. Our fi ndings stress the importance to interpret a positive CCP test carefully when evaluated in non-rheumatic conditions or in areas where such infections predominate. |
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| 4. | Mem Inst Oswaldo Cruz. 2011 Nov;106(7):856-63.Schistosoma mansoni antigens alter the cytokine response in vitro during cutaneous leishmaniasis.Bafica AM, Cardoso LS, Oliveira SC, Loukas A, Varela GT, Oliveira RR, Bacellar O, Carvalho EM, Araújo MI.SourceServiço de Imunologia, Hospital Universitário Professor Edgard Santos, Universidade Federal da Bahia, Salvador, BA, Brasil. AbstractSchistosoma mansoni infection or associated products are able to down-modulate the type 1 CD4+ T cell inflammatory response characteristic of autoimmune diseases. In this study, we evaluated how S. mansoni antigens altered the immune response that was induced by the soluble Leishmania antigen (SLA) from cutaneous leishmaniasis (CL) patients. Cytokines were measured from the supernatants of peripheral blood mononuclear cell cultures stimulated with SLA. This was performed using the sandwich enzyme linked immunosorbent assay technique in the presence or absence of S. mansoni recombinant antigens Sm29, SmTSP-2 and PIII. The addition of S. mansoni antigens to the cultures resulted in the reduction of interferon gamma (IFN-γ) levels in 37-50% of patients. Although to a lesser extent, the antigens were also able to decrease the production of tumour necrosis factor-alpha (TNF-α). We compared patients that either had or did not have reduction in IFN-γ and TNF-α production in cultures stimulated with SLA in the presence of S. mansoni antigens. We found that there was no significant difference in the levels of interleukin (IL)-10 and IL-5 in response to S. mansoni antigens between the groups. The antigens used in this study down-modulated the in vitro proinflammatory response induced by SLA in a group of CL patients through a currently undefined mechanism. |
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| 5. | Cad Saude Publica. 2011 Nov;27(11):2117-23.Assessment of sand fly (Diptera, Psychodidae) control using cypermethrin in an endemic area for visceral leishmaniasis, Montes Claros, Minas Gerais State, Brazil.Barata RA, Michalsky EM, Fujiwara RT, França-Silva JC, Rocha MF, Dias ES.SourceUniversidade Federal dos Vales do Jequitinhonha e Mucuri, Diamantina, Brasil. AbstractMontes Claros in Minas Gerais State, Brazil, was considered an intense transmission area for visceral leishmaniasis. This study evaluated sand fly fauna after insecticide application. Captures were performed in 10 districts from September 2005 to August 2006 with CDC light traps inside and outside each residence. Cypermethrin was sprayed in two cycles during November/2005 and May/2006. The 636 specimens collected, belonging to 10 species, were predominantly Lutzomyia longipalpis (79%), and most frequently males (70%). The highest percentage of specimens were captured in areas surrounding domiciles (85.8%). The main species were observed to be sensitive to treatment with the insecticide. The results showed a reduction in the number of sand flies collected after use of cypermethrin in homes and annexes, and with residual effect lasting from two to four months. |
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| 6. | Immunol Cell Biol. 2011 Nov 29. doi: 10.1038/icb.2011.97. [Epub ahead of print]HDAC inhibitors in parasitic diseases.Andrews KT, Haque A, Jones MK.Source1] Eskitis Institute for Cell and Molecular Therapies, Griffith University, Nathan, Queensland, Australia [2] Queensland Institute of Medical Research, Herston, Queensland, Australia. AbstractParasitic diseases cause significant global morbidity and mortality, particularly in underdeveloped regions of the world. Malaria alone causes ∼800 000 deaths each year, with children and pregnant women being at highest risk. There is no licensed vaccine available for any human parasitic disease and drug resistance is compromising the efficacy of many available anti-parasitic drugs. This is driving drug discovery research on new agents with novel modes of action. Histone deacetylase (HDAC) inhibitors are being investigated as drugs for a range of diseases, including cancers and infectious diseases such as HIV/AIDS, and several parasitic diseases. This review focuses on the current state of knowledge of HDAC inhibitors targeted to the major human parasitic diseases malaria, schistosomiasis, trypanosomiasis, toxoplasmosis and leishmaniasis. Insights are provided into the unique challenges that will need to be considered if HDAC inhibitors are to be progressed towards clinical development as potential new anti-parasitic drugs.Immunology and Cell Biology advance online publication, 29 November 2011; doi:10.1038/icb.2011.97. |
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| 7. | Chem Commun (Camb). 2011 Nov 28. [Epub ahead of print]Proteomic profiling and potential cellular target identification of K11777, a clinical cysteine protease inhibitor, in Trypanosoma brucei.Yang PY, Wang M, He CY, Yao SQ.SourceDepartment of Chemistry, National University of Singapore, 3 Science Drive 3, Singapore117543. chmyaosq@nus.edu.sg. AbstractWe report herein the design, synthesis and application of K11777-derived activity-based probes (ABPs) allowing in situ profiling and identification of potential cellular targets of K11777 in Trypanosoma brucei. |
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| 8. | Antimicrob Agents Chemother. 2011 Nov 28. [Epub ahead of print]Mechanism of Amphotericin B Resistance in Clinical Isolates of L eishmania donovani.Purkait B, Kumar A, Nandi N, Sardar AH, Das S, Kumar S, Pandey K, Ravidas V, Kumar M, De T, Singh D, Das P.SourceDepartment of Molecular Biology. AbstractThe clinical value of Amphotericin B, the mainstay therapy for Visceral Leishmaniasis in Sodium Antimony Gluconate nonresponsive zones of Bihar, is now threatened by the emergence of acquired drug resistance and a comprehensive understanding of the underlying mechanisms is the need of the hour. We have selected an Amphotericin B resistant clinical isolate which demonstrated 8 fold higher LD(50) compared to sensitive strain to explore the mechanism of Amphotericin B resistance. Fluoremetric analysis demonstrated lower anisotropy in the motion of the diphenylhexatriene fluorescent probe, which indicated a higher fluidity of the membrane of resistant strain compared to sensitive. The expression pattern of the two transcripts of S-adenosyl-L-methionine-C24-Δ-sterolmethyltransferase and the absence of ergosterol replaced by cholesta-5, 7, 24-triene-3β-ol in the membrane of the resistant parasite indicates toward the decreased Amphotericin B affinity for same which is evidenced by decreased Amphotericin B uptake. The expression level of MDR1 is found to be higher in the resistant strain suggesting a higher rate of efflux of Amphotericin B. The resistant parasite also possess an upregulated tryparedoxin cascade and higher reduced intracellular thiol level which helps in better scavenging of Reactive Oxygen Species produced by Amphotericin B. The resistance to Amphotericin B was partially reverted by thiol metabolic pathway and ABC transporter inhibitors. Thus, it can be concluded that altered membrane composition, ATP-binding cassette transporters and an upregulated thiol metabolic pathway have a role in conferring Amphotericin B resistance in clinical isolates of L. donovani. |
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| 9. | Antimicrob Agents Chemother. 2011 Nov 28. [Epub ahead of print]Efficacy of synthetic peptides RP-1 and AA-RP-1 against Leishmania species in vi tro and in vivo.Erfe MC, David CV, Huang C, Lu V, Maretti-Mira AC, Haskell J, Bruhn KW, Yeaman MR, Craft N.SourceLos Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA. AbstractHost defense peptides are naturally-occurring molecules that play essential roles in innate immunity to infection. Based on prior structure-function knowledge, we tested two synthetic peptides (RP-1 and AA-RP-1) modeled on the conserved, microbicidal α-helical domain of mammalian CXCL4 platelet kinocidins. These peptides were evaluated for efficacy against Leishmania species, the causative agents of the group of diseases known as leishmaniasis. In vitro anti-leishmanial activity was assessed against three distinct Leishmania strains by measuring proliferation, metabolic activity and parasite viability after exposure to varying concentrations of peptides. We demonstrate that micromolar concentrations of RP-1 and AA-RP-1 caused dose-dependent growth inhibition of Leishmania promastigotes. This anti-leishmanial activity correlated with rapid membrane disruption as well as a loss of mitochondrial transmembrane potential. Additionally, RP-1 and AA-RP-1 demonstrated distinct and significant in vivo anti-leishmanial activities in a mouse model of experimental visceral leishmaniasis after intravenous administration. These results establish efficacy of RP-1 lineage synthetic peptides against Leishmania species in vitro and following intravenous administration in vivo, and provide further validation of proof-of-concept for development of these and related systemic anti-infective peptides targeting pathogens that are resistant to conventional antibiotics. |
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| 10. | Ann Biol Clin (Paris). 2011 Dec 1;69(6):729-731.Association of acute lymphoblastic leukaemia and visceral leishmaniasis .Nafil H, Tazi I, Mahmal L.SourceService d'hématologie, CHU Mohamed VI, Université Cadi Ayyad, Marrakech, Maroc. AbstractVisceral leishmaniasis (VL) can be regarded as a rare opportunistic infection in patients with acute lymphoblastic leukemia (ALL). We report the case of a 20-year-old woman treated for ALL. During maintenance treatment, the patient presents with pallor, prolonged fever and asthenia. The examination objective splenomegaly and blood counts showed pancytopenia. The bone marrow aspiration confirmed the diagnosis of VL. The patient was treated with antimoniate of meglumine with good evolution. |
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