Deletion of the Aryl Hydrocarbon Receptor Enhances the Inflammatory Response to Leishmania major Infection


Por: Elizondo G., Rodríguez-Sosa M., Estrada-Muñiz E., Gonzalez F.J., Vega L.

Publicada: 1 ene 2011
Resumen:
The aryl hydrocarbon receptor (AhR) is a ligand-activated receptor that mediates the toxicity of environmental pollutants, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Recently, it has been shown that the AhR plays a role in immune and inflammatory regulation. However, most of these studies are based on the activation of AhR by exogenous ligands. Therefore, in the present study, we addressed the role of this transcription factor, in the absent of exogenous ligand, on the immune response to Leishmania major infection. Our results indicate that inactivation of the AhR results in an alteration of the levels of several cytokines. Lymph node cells from infected Ahr-null animals displayed an increase in IFN gamma and IL-12 levels, together with a decrease in IL-4 and IL-10 levels compared to wild-type (wt) mice. Ahr-null mice also presented higher serum levels of the pro-inflammatory cytokine TNF-alpha prior to parasite inoculation and during infection compared to wt mice. Moreover, a

Filiaciones:
Elizondo G.:
 Centro de Investigación y Estudios Avanzados, Instituto Politécnico Nacional, Departamento de Biología Celular, Av. IPN 2508. San Pedro Zacatenco, C. P. 07360, México D. F., Mexico

Rodríguez-Sosa M.:
 UNAM, Fac Estudios Super Iztacala, Unidad Biomed, Tlalnepantla 54090, Estado De Mexic, Mexico

Estrada-Muñiz E.:
 Centro de Investigación y Estudios Avanzados, Instituto Politécnico Nacional, Departamento de Toxicología, Av. IPN 2508. San Pedro Zacatenco, C. P. 07360, México D. F., Mexico

Gonzalez F.J.:
 Laboratory of Metabolism, NCI, National Institutes of Health, Bethesda, MD 20892, United States

Vega L.:
 Centro de Investigación y Estudios Avanzados, Instituto Politécnico Nacional, Departamento de Toxicología, Av. IPN 2508. San Pedro Zacatenco, C. P. 07360, México D. F., Mexico
ISSN: 14492288
Editorial
IVYSPRING INT PUBL, PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA, Australia
Tipo de documento: Article
Volumen: 7 Número: 9
Páginas: 1220-1229
WOS Id: 000298011000002
ID de PubMed: 22110376
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