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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 505694, 15 pages
http://dx.doi.org/10.1155/2010/505694
Research Article

The Unexpected Role for the Aryl Hydrocarbon Receptor on Susceptibility to Experimental Toxoplasmosis

1Unidad de Biomedicina, Facultad de Estudios Superiores-Iztacala, Universidad Nacional Autónoma de México (UNAM), CP 54090, o. Tlalnepantla, Edo. de México, Mexico
2Departamento de Toxicología, Centro de Investigación y Estudios Avanzados-IPN, Avenue IPN 2508, San Pedro Zacatenco, CP 07360 México, DF, Mexico
3Departamento de Biología Celular, Centro de Investigación y Estudios Avanzados-IPN, Avenue IPN 2508, San Pedro Zacatenco, CP 07360 México, DF, Mexico
4Depertamento de inmunología, Instituto de Investigaciones Biomédicas, UNAM, México, DF, Mexico

Received 20 August 2009; Accepted 15 October 2009

Academic Editor: Luis I. Terrazas

Copyright © 2010 Yuriko Sanchez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The aryl hydrocarbon receptor (AhR) is part of a signaling system that is mainly triggered by xenobiotic agents. Increasing evidence suggests that AhR may regulate immunity to infections. To determine the role of AhR in the outcome of toxoplasmosis, we used AhR-/- and wild-type (WT) mice. Following an intraperitoneal infection with Toxoplasma gondii (T. gondii), AhR-/- mice succumbed significantly faster than WT mice and displayed greater liver damage as well as higher serum levels of tumor necrosis factor (TNF)- 𝛼 , nitric oxide (NO), and IgE but lower IL-10 secretion. Interestingly, lower numbers of cysts were found in their brains. Increased mortality was associated with reduced expression of GATA-3, IL-10, and 5-LOX mRNA in spleen cells but higher expression of IFN- 𝛾 mRNA. Additionally, peritoneal exudate cells from AhR-/- mice produced higher levels of IL-12 and IFN- 𝛾 but lower TLR2 expression than WT mice. These findings suggest a role for AhR in limiting the inflammatory response during toxoplasmosis.