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BioMed Research International
Volume 2013 (2013), Article ID 696343, 11 pages
http://dx.doi.org/10.1155/2013/696343
Research Article

Signal Transducer and Activator of Transcription Factor 6 Signaling Contributes to Control Host Lung Pathology but Favors Susceptibility against Toxocara canis Infection

1Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Avenue de los Barrios 1, Los Reyes Iztacala, Tlalnepantla 54090, MEX, Mexico City, DE, Mexico
2Laboratorio de Parasitología, Facultad de Estudios Superiores Cuautitlán, UNAM, 54714 Mexico City, DE, Mexico
3Laboratorio de Histopatología, Facultad de Estudios Superiores Cuautitlán, UNAM, 54714 Mexico City, DE, Mexico
4Carrera de Medicina, Facultad de Estudios Superiores Iztacala, UNAM, 54090 Mexico City, DE, Mexico

Received 10 August 2012; Accepted 29 October 2012

Academic Editor: Miriam Rodríguez-Sosa

Copyright © 2013 Berenice Faz-López 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

Using BALB/c mice, we have analyzed the role of STAT6-induced Th2 response in determining the outcome of experimental toxocariasis caused by embryonated eggs of the helminth parasite Toxocara canis. Following T. canis infection wild-type BALB/c mice developed a strong Th2-like response, produced high levels of IgG1, IgE, and IL-4, recruited alternatively activated macrophages, and displayed a moderate pathology in the lungs; however, they harbored heavy parasite loads in different tissues. In contrast, similarly infected BALB/c mice mounted a weak Th2-like response, did not recruit alternatively activated macrophages, displayed a severe pathology in the lungs, but efficiently controlled T. canis infection. These findings demonstrate that Th2-like response induced via STAT6-mediated signaling pathway mediates susceptibility to larval stage of T. canis. Furthermore, they also indicate that unlike most gastrointestinal helminths, immunity against larvae of T. canis is not mediated by a Th2-dominant response.