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  1. Article ; Online: Plasmodium berghei ANKA (PbA) infection of C57BL/6J mice: a model of severe malaria.

    de Oca, Marcela Montes / Engwerda, Christian / Haque, Ashraful

    Methods in molecular biology (Clifton, N.J.)

    2013  Volume 1031, Page(s) 203–213

    Abstract: The term "severe malaria" refers to a wide spectrum of syndromes in Plasmodium-infected humans including cerebral malaria (CM), respiratory distress, severe anemia, liver dysfunction, and hypoglycemia. Mouse models have been employed to further our ... ...

    Abstract The term "severe malaria" refers to a wide spectrum of syndromes in Plasmodium-infected humans including cerebral malaria (CM), respiratory distress, severe anemia, liver dysfunction, and hypoglycemia. Mouse models have been employed to further our understanding of the pathology and immune responses that occur during Plasmodium infection. Evidence of brain, liver, lung, and spleen pathology, as well as anemia and tissue-sequestration of parasites, has been reported in various strains of inbred mice. While no single mouse model mimics all the various clinical manifestations of severe malaria in humans, here we describe a detailed protocol for Plasmodium berghei ANKA infection of C57BL/6J mice. For many years, this model has been referred to as "experimental cerebral malaria," but in fact recapitulates many of the symptoms and pathologies observed in most severe malaria syndromes.
    MeSH term(s) Animals ; Brain/parasitology ; Brain/pathology ; Disease Models, Animal ; Humans ; Liver/parasitology ; Liver/pathology ; Liver Diseases/parasitology ; Liver Diseases/pathology ; Lung/parasitology ; Lung/pathology ; Malaria/genetics ; Malaria/parasitology ; Malaria/pathology ; Mice ; Mice, Inbred C57BL ; Plasmodium berghei/genetics ; Plasmodium berghei/pathogenicity ; Spleen/parasitology ; Spleen/pathology
    Language English
    Publishing date 2013
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-62703-481-4_23
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The Role of BACH2 in T Cells in Experimental Malaria Caused by

    Edwards, Chelsea L / de Oca, Marcela Montes / de Labastida Rivera, Fabian / Kumar, Rajiv / Ng, Susanna S / Wang, Yulin / Amante, Fiona H / Kometani, Kohei / Kurosaki, Tomohiro / Sidwell, Tom / Kallies, Axel / Engwerda, Christian R

    Frontiers in immunology

    2018  Volume 9, Page(s) 2578

    Abstract: BTB and CNC Homology 1, Basic Leucine Zipper Transcription Factor 2 (BACH2) is a transcription factor best known for its role in B cell development. More recently, it has been associated with T cell functions in inflammatory diseases, and has been ... ...

    Abstract BTB and CNC Homology 1, Basic Leucine Zipper Transcription Factor 2 (BACH2) is a transcription factor best known for its role in B cell development. More recently, it has been associated with T cell functions in inflammatory diseases, and has been proposed as a master transcriptional regulator within the T cell compartment. In this study, we employed T cell-specific
    MeSH term(s) Animals ; Basic-Leucine Zipper Transcription Factors/genetics ; Basic-Leucine Zipper Transcription Factors/metabolism ; Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Chimera ; Female ; Humans ; Lymphocyte Activation ; Malaria/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Animal ; Plasmodium chabaudi/physiology ; Th17 Cells/immunology ; Th2 Cells/immunology
    Chemical Substances Bach2 protein, mouse ; Basic-Leucine Zipper Transcription Factors
    Language English
    Publishing date 2018-11-06
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2018.02578
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Spatiotemporal requirements for IRF7 in mediating type I IFN-dependent susceptibility to blood-stage Plasmodium infection.

    Edwards, Chelsea L / Best, Shannon E / Gun, Sin Yee / Claser, Carla / James, Kylie R / de Oca, Marcela Montes / Sebina, Ismail / Rivera, Fabian de Labastida / Amante, Fiona H / Hertzog, Paul J / Engwerda, Christian R / Renia, Laurent / Haque, Ashraful

    European journal of immunology

    2015  Volume 45, Issue 1, Page(s) 130–141

    Abstract: Type I IFN signaling suppresses splenic T helper 1 (Th1) responses during blood-stage Plasmodium berghei ANKA (PbA) infection in mice, and is crucial for mediating tissue accumulation of parasites and fatal cerebral symptoms via mechanisms that remain to ...

    Abstract Type I IFN signaling suppresses splenic T helper 1 (Th1) responses during blood-stage Plasmodium berghei ANKA (PbA) infection in mice, and is crucial for mediating tissue accumulation of parasites and fatal cerebral symptoms via mechanisms that remain to be fully characterized. Interferon regulatory factor 7 (IRF7) is considered to be a master regulator of type I IFN responses. Here, we assessed IRF7 for its roles during lethal PbA infection and nonlethal Plasmodium chabaudi chabaudi AS (PcAS) infection as two distinct models of blood-stage malaria. We found that IRF7 was not essential for tissue accumulation of parasites, cerebral symptoms, or brain pathology. Using timed administration of anti-IFNAR1 mAb, we show that late IFNAR1 signaling promotes fatal disease via IRF7-independent mechanisms. Despite this, IRF7 significantly impaired early splenic Th1 responses and limited control of parasitemia during PbA infection.  Finally, IRF7 also suppressed antiparasitic immunity and Th1 responses during nonlethal PcAS infection. Together, our data support a model in which IRF7 suppresses antiparasitic immunity in the spleen, while IFNAR1-mediated, but IRF7-independent, signaling contributes to pathology in the brain during experimental blood-stage malaria.
    MeSH term(s) Animals ; Antibodies, Monoclonal/pharmacology ; Brain/drug effects ; Brain/immunology ; Brain/parasitology ; Disease Susceptibility ; Erythrocytes/parasitology ; Female ; Gene Expression Regulation ; Host-Parasite Interactions ; Interferon Regulatory Factor-7/genetics ; Interferon Regulatory Factor-7/immunology ; Malaria, Cerebral/immunology ; Malaria, Cerebral/parasitology ; Mice ; Mice, Inbred C57BL ; Plasmodium berghei/immunology ; Plasmodium chabaudi/immunology ; Receptor, Interferon alpha-beta/antagonists & inhibitors ; Receptor, Interferon alpha-beta/genetics ; Receptor, Interferon alpha-beta/immunology ; Signal Transduction ; Spleen/drug effects ; Spleen/immunology ; Spleen/parasitology ; Th1 Cells/immunology ; Th1 Cells/parasitology ; Time Factors
    Chemical Substances Antibodies, Monoclonal ; Ifnar1 protein, mouse ; Interferon Regulatory Factor-7 ; Irf7 protein, mouse ; Receptor, Interferon alpha-beta (156986-95-7)
    Language English
    Publishing date 2015-01
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.201444824
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 489: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 85: Show issues

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  4. Article ; Online: Type I interferons suppress CD4⁺ T-cell-dependent parasite control during blood-stage Plasmodium infection.

    Haque, Ashraful / Best, Shannon E / Ammerdorffer, Anne / Desbarrieres, Laure / de Oca, Marcela Montes / Amante, Fiona H / de Labastida Rivera, Fabian / Hertzog, Paul / Boyle, Glen M / Hill, Geoffrey R / Engwerda, Christian R

    European journal of immunology

    2011  Volume 41, Issue 9, Page(s) 2688–2698

    Abstract: During blood-stage Plasmodium infection, large-scale invasion of RBCs often occurs before the generation of cellular immune responses. In Plasmodium berghei ANKA (PbA)-infected C57BL/6 mice, CD4(+) T cells controlled parasite numbers poorly, instead ... ...

    Abstract During blood-stage Plasmodium infection, large-scale invasion of RBCs often occurs before the generation of cellular immune responses. In Plasmodium berghei ANKA (PbA)-infected C57BL/6 mice, CD4(+) T cells controlled parasite numbers poorly, instead providing early help to pathogenic CD8(+) T cells. Expression analysis revealed that the transcriptional signature of CD4(+) T cells from PbA-infected mice was dominated by type I IFN (IFN-I) and IFN-γ-signalling pathway-related genes. A role for IFN-I during blood-stage Plasmodium infection had yet to be established. Here, we observed IFN-α protein production in the spleen of PbA-infected C57BL/6 mice over the first 2 days of infection. Mice deficient in IFN-I signalling had reduced parasite burdens, and displayed none of the fatal neurological symptoms associated with PbA infection. IFN-I substantially inhibited CD4(+) T-bet(+) T-cell-derived IFN-γ production, and prevented this emerging Th1 response from controlling parasites. Experiments using BM chimeric mice revealed that IFN-I signalled predominantly via radio-sensitive, haematopoietic cells, but did not suppress CD4(+) T cells via direct signalling to this cell type. Finally, we found that IFN-I suppressed IFN-γ production, and hampered efficient control of parasitaemia in mice infected with non-lethal Plasmodium chabaudi. Thus, we have elucidated a novel regulatory pathway in primary blood-stage Plasmodium infection that suppresses CD4(+) T-cell-mediated parasite control.
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/parasitology ; CD8-Positive T-Lymphocytes/pathology ; Cells, Cultured ; Immune Evasion ; Immunosuppression ; Interferon Type I/immunology ; Interferon Type I/metabolism ; Interferon-gamma/secretion ; Life Cycle Stages ; Malaria/immunology ; Mice ; Mice, Inbred C57BL ; Plasmodium berghei/immunology ; Plasmodium berghei/pathogenicity ; Plasmodium chabaudi/immunology ; Plasmodium chabaudi/pathogenicity ; Signal Transduction/immunology ; T-Box Domain Proteins/metabolism ; Th1 Cells/immunology ; Th1 Cells/metabolism ; Th1 Cells/parasitology ; Th1 Cells/pathology ; Transplantation Chimera ; Virulence
    Chemical Substances Interferon Type I ; T-Box Domain Proteins ; T-box transcription factor TBX21 ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2011-09
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.201141539
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 489: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 85: Show issues

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  5. Article ; Online: Acute Renal Failure Induced by Choline Deficiency

    de Oca, Marcela Montes / Perazzo, Juan C. / Monserrat, Alberto J. / de Muchnik, Elvira E. Arrizurieta

    Nephron

    1980  Volume 26, Issue 1, Page(s) 41–48

    Abstract: The wide range of lesions obtained after feeding weanling rats with hypolipotropic diets underlies the interest of this model in the study of the pathophysiology of acute renal failure. Renal functional studies (experiment A) show that the more advanced ... ...

    Abstract The wide range of lesions obtained after feeding weanling rats with hypolipotropic diets underlies the interest of this model in the study of the pathophysiology of acute renal failure. Renal functional studies (experiment A) show that the more advanced grade of morphological alteration correlates well with a progressively more severe deterioration in renal function. In animals with morphological evidence of repair there was an evident rise in the urinary volume of a low osmolality and a reduction in blood urea. In experiment B, where the sequential changes in urine volume and composition were analyzed, the installation of the disease is marked by a decrease in body weight, food intake and water intake, a rise in urine Na concentration and by a fall in urine flow rate and renal capacity to excrete concentrated urine. The progressive decline in renal function observed in these animals would seem more linked to a primary tubular alteration which gradually becomes more extensive than with an initial ischemic alteration. The tubular necrosis can be interpreted as the initial lesion common to the wide morphological range observed in this model (tubular necrosis of various grades, cortical necrosis or evidence of repair).
    Keywords Acute renal failure ; Choline deficiency ; Acute tubular necrosis ; Cortical necrosis ; Hypolipotropic diets
    Language English
    Publisher S. Karger AG
    Publishing place Basel
    Publishing country Switzerland
    Document type Article ; Online
    ZDB-ID 207121-6
    ISSN 1423-0186 ; 0028-2766 ; 1660-8151 ; 0028-2766 ; 1660-8151
    ISSN (online) 1423-0186
    ISSN 0028-2766 ; 1660-8151
    DOI 10.1159/000181948
    Database Karger publisher's database

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 169: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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