UCP2 deficiency helps to restrict the pathogenesis of experimental cutaneous and visceral leishmaniosis in mice

Autor: M. Angeles Abengozar, Carlos Sanchez-Martin, M. Mar González-Barroso, Javier Carrión, María José Fernández-Reyes, Gustavo Domínguez-Bernal, Eduardo Rial
Jazyk: angličtina
Rok vydání: 2013
Předmět:
Mouse
medicine.medical_treatment
Ion Channels
Parasite Load
Pathogenesis
Mice
Zoonoses
Parasite hosting
Uncoupling Protein 2
Leishmania infantum
Leishmaniasis
Leishmania major
chemistry.chemical_classification
Mice
Knockout
biology
lcsh:Public aspects of medicine
Animal Models
Host-Pathogen Interaction
Cytokine
Infectious Diseases
Cytokines
Leishmaniasis
Visceral
Medicine
Female
Research Article
Neglected Tropical Diseases
lcsh:Arctic medicine. Tropical medicine
lcsh:RC955-962
Immunology
Leishmaniasis
Cutaneous
Microbiology
Mitochondrial Proteins
Model Organisms
Downregulation and upregulation
medicine
Parasitic Diseases
Animals
Biology
Microbial Pathogens
Reactive oxygen species
Intracellular parasite
Public Health
Environmental and Occupational Health
Transporter
lcsh:RA1-1270
Leishmania
biology.organism_classification
Mice
Inbred C57BL
Disease Models
Animal
chemistry
Parasitology
Veterinary Science
Zdroj: PLoS Neglected Tropical Diseases, Vol 7, Iss 2, p e2077 (2013)
PLoS Neglected Tropical Diseases
Digital.CSIC. Repositorio Institucional del CSIC
instname
ISSN: 1935-2735
1935-2727
Popis: 10 p.-4 fig.3 tab.
BACKGROUND: 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). METHODOLOGY AND FINDINGS: 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-¿ (IFN-¿), IL-17 and IL-13 than WT mice (P
This research was supported in part by grants AGL2010-17394, ISCIII PI09-01928 and Consolider-Ingenio 2010 (CSD2007-00020) from the Spanish Ministry of Education and Science (MEC). MMGB and JC were supported by a ‘‘Ramo´n y Cajal’’ contract and a ‘‘Juan de la Cierva’’ (JCI-2009-04069) contract,respectively, from the Ministry of Economy and Competitiveness (formerly MEC). Funding from the grant RICET RD 06/0021/0006 is also gratefully acknowledged.
Databáze: OpenAIRE
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