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  1. Article: Metabolic Adaptation to Tissue Iron Overload Confers Tolerance to Malaria

    Gozzelino, Raffaella / Andrade, Bruno Bezerril / Larsen, Rasmus / Luz, Nivea F / Vanoaica, Liviu / Seixas, Elsa / Coutinho, Antonio / Cardoso, Sílvia / Rebelo, Sofia / Poli, Maura / Barral-Netto, Manoel / Darshan, Deepak / Kühn, Lukas C / Soares, Miguel P

    Cell host & microbe. 2012 Nov. 15, v. 12, no. 5

    2012  

    Abstract: Disease tolerance is a defense strategy that limits the fitness costs of infection irrespectively of pathogen burden. While restricting iron (Fe) availability to pathogens is perceived as a host defense strategy, the resulting tissue Fe overload can be ... ...

    Abstract Disease tolerance is a defense strategy that limits the fitness costs of infection irrespectively of pathogen burden. While restricting iron (Fe) availability to pathogens is perceived as a host defense strategy, the resulting tissue Fe overload can be cytotoxic and promote tissue damage to exacerbate disease severity. Examining this interplay during malaria, the disease caused by Plasmodium infection, we find that expression of the Fe sequestering protein ferritin H chain (FtH) in mice, and ferritin in humans, is associated with reduced tissue damage irrespectively of pathogen burden. FtH protection relies on its ferroxidase activity, which prevents labile Fe from sustaining proapoptotic c-Jun N-terminal kinase (JNK) activation. FtH expression is inhibited by JNK activation, promoting tissue Fe overload, tissue damage, and malaria severity. Mimicking FtH’s antioxidant effect or inhibiting JNK activation pharmacologically confers therapeutic tolerance to malaria in mice. Thus, FtH provides metabolic adaptation to tissue Fe overload, conferring tolerance to malaria.
    Keywords Plasmodium ; antioxidant activity ; apoptosis ; cytotoxicity ; disease resistance ; disease severity ; ferritin ; ferroxidase ; humans ; iron ; iron overload ; malaria ; mice ; mitogen-activated protein kinase ; pathogens
    Language English
    Dates of publication 2012-1115
    Size p. 693-704.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 2278004-X
    ISSN 1931-3128
    ISSN 1931-3128
    DOI 10.1016/j.chom.2012.10.011
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Cologne/Königswinter

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  2. Article ; Online: Gut Microbiota Elicits a Protective Immune Response against Malaria Transmission

    Yilmaz, Bahtiyar / Portugal, Silvia / Tran, Tuan M. / Gozzelino, Raffaella / Ramos, Susana Amaral / Gomes, Joana / Regalado, Ana / Cowan, Peter J. / d’Apice, Anthony J.F. / Chong, Anita S. / Doumbo, Ogobara K. / Traoré, Boubacar / Crompton, Peter D. / Silveira, Henrique / Soares, Miguel P.

    Cell. 2014 Dec. 04, v. 159 p.1277-1289

    2014  

    Abstract: Glycosylation processes are under high natural selection pressure, presumably because these can modulate resistance to infection. Here, we asked whether inactivation of the UDP-galactose:β-galactoside-α1-3-galactosyltransferase (α1,3GT) gene, which ... ...

    Abstract Glycosylation processes are under high natural selection pressure, presumably because these can modulate resistance to infection. Here, we asked whether inactivation of the UDP-galactose:β-galactoside-α1-3-galactosyltransferase (α1,3GT) gene, which ablated the expression of the Galα1-3Galβ1-4GlcNAc-R (α-gal) glycan and allowed for the production of anti-α-gal antibodies (Abs) in humans, confers protection against Plasmodium spp. infection, the causative agent of malaria and a major driving force in human evolution. We demonstrate that both Plasmodium spp. and the human gut pathobiont E. coli O86:B7 express α-gal and that anti-α-gal Abs are associated with protection against malaria transmission in humans as well as in α1,3GT-deficient mice, which produce protective anti-α-gal Abs when colonized by E. coli O86:B7. Anti-α-gal Abs target Plasmodium sporozoites for complement-mediated cytotoxicity in the skin, immediately after inoculation by Anopheles mosquitoes. Vaccination against α-gal confers sterile protection against malaria in mice, suggesting that a similar approach may reduce malaria transmission in humans.[Display omitted]
    Keywords Anopheles ; Escherichia coli ; Plasmodium ; antibodies ; complement ; cytotoxicity ; digestive system ; genes ; glycosylation ; humans ; immune response ; intestinal microorganisms ; malaria ; mice ; natural selection ; selection pressure ; sporozoites ; vaccination
    Language English
    Dates of publication 2014-1204
    Size p. 1277-1289.
    Publishing place Elsevier Inc.
    Document type Article ; Online
    Note Resource is Open Access
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2014.10.053
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

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  3. Article: Sickle Hemoglobin Confers Tolerance to Plasmodium Infection

    Ferreira, Ana / Marguti, Ivo / Bechmann, Ingo / Jeney, Viktória / Chora, Ângelo / Palha, Nuno R. / Rebelo, Sofia / Henri, Annie / Beuzard, Yves / Soares, Miguel P.

    Cell

    Volume v. 145,, Issue no. 3

    Abstract: Sickle human hemoglobin (Hb) confers a survival advantage to individuals living in endemic areas of malaria, the disease caused by Plasmodium infection. As demonstrated hereby, mice expressing sickle Hb do not succumb to experimental cerebral malaria ( ... ...

    Abstract Sickle human hemoglobin (Hb) confers a survival advantage to individuals living in endemic areas of malaria, the disease caused by Plasmodium infection. As demonstrated hereby, mice expressing sickle Hb do not succumb to experimental cerebral malaria (ECM). This protective effect is exerted irrespectively of parasite load, revealing that sickle Hb confers host tolerance to Plasmodium infection. Sickle Hb induces the expression of heme oxygenase-1 (HO-1) in hematopoietic cells, via a mechanism involving the transcription factor NF-E2-related factor 2 (Nrf2). Carbon monoxide (CO), a byproduct of heme catabolism by HO-1, prevents further accumulation of circulating free heme after Plasmodium infection, suppressing the pathogenesis of ECM. Moreover, sickle Hb inhibits activation and/or expansion of pathogenic CD8⁺ T cells recognizing antigens expressed by Plasmodium, an immunoregulatory effect that does not involve Nrf2 and/or HO-1. Our findings provide insight into molecular mechanisms via which sickle Hb confers host tolerance to severe forms of malaria.
    Keywords parasite load ; CD8-positive T-lymphocytes ; metabolism ; heme ; transcription factors ; pathogenesis ; humans ; protective effect ; abnormal hemoglobin ; mice ; carbon monoxide ; Plasmodium ; hematopoietic stem cells ; cerebral malaria ; heme oxygenase (biliverdin-producing) ; antigens
    Language English
    Document type Article
    ISSN 0092-8674
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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