UCP2 deficiency helps to restrict the pathogenesis of experimental cutaneous and visceral leishmaniosis in mice.
| Autor: | Javier Carrión, M Angeles Abengozar, María Fernández-Reyes, Carlos Sánchez-Martín, Eduardo Rial, Gustavo Domínguez-Bernal, M Mar González-Barroso |
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| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: | |
| Zdroj: | PLoS Neglected Tropical Diseases, Vol 7, Iss 2, p e2077 (2013) |
| Druh dokumentu: | article |
| ISSN: | 1935-2727 1935-2735 |
| DOI: | 10.1371/journal.pntd.0002077 |
| Popis: | Uncoupling protein 2 (UCP2) is a mitochondrial transporter that has been shown to lower the production of reactive oxygen species (ROS). Intracellular pathogens such as Leishmania upregulate UCP2 and thereby suppress ROS production in infected host tissues, allowing the multiplication of parasites within murine phagocytes. This makes host UCP2 and ROS production potential targets in the development of antileishmanial therapies. Here we explore how UCP2 affects the outcome of cutaneous leishmaniosis (CL) and visceral leishmaniosis (VL) in wild-type (WT) C57BL/6 mice and in C57BL/6 mice lacking the UCP2 gene (UCP2KO).To investigate the effects of host UCP2 deficiency on Leishmania infection, we evaluated parasite loads and cytokine production in target organs. Parasite loads were significantly lower in infected UCP2KO mice than in infected WT mice. We also found that UCP2KO mice produced significantly more interferon-γ (IFN-γ), IL-17 and IL-13 than WT mice (P |
| Databáze: | Directory of Open Access Journals |
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