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Interleukin-25 Induces Resistance Against Intestinal Trematodes

Echinostoma caproni is an intestinal trematode that has been extensively used as an experimental model to investigate the factors determining the resistance to intestinal helminths or the development of chronic infections. ICR mice are permissive hosts for E. caproni in which chronic infections are...

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Autores principales: Muñoz-Antoli, Carla, Cortés, Alba, Santano, Rebeca, Sotillo, Javier, Esteban, J. Guillermo, Toledo, Rafael
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5034261/
https://www.ncbi.nlm.nih.gov/pubmed/27658962
http://dx.doi.org/10.1038/srep34142
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author Muñoz-Antoli, Carla
Cortés, Alba
Santano, Rebeca
Sotillo, Javier
Esteban, J. Guillermo
Toledo, Rafael
author_facet Muñoz-Antoli, Carla
Cortés, Alba
Santano, Rebeca
Sotillo, Javier
Esteban, J. Guillermo
Toledo, Rafael
author_sort Muñoz-Antoli, Carla
collection PubMed
description Echinostoma caproni is an intestinal trematode that has been extensively used as an experimental model to investigate the factors determining the resistance to intestinal helminths or the development of chronic infections. ICR mice are permissive hosts for E. caproni in which chronic infections are developed, concomitantly with local Th1 responses, elevated levels of local IFN-γ, inflammation and antibody responses. However, mice develop partial resistance to homologous challenge infections after cure of a primary infection, which converts this subject into an adequate model for the study of the mechanisms generating resistance against intestinal helminths. The purpose of the present study was to compare the immune response induced in primary and secondary infections to elucidate the factors determining the different outcome of the infection in each type of infection. The results obtained indicate that susceptibility is determined by the lack of IL-25 expression in response to primary infection. In contrast, infection in an environment with elevated levels of IL-25, as occurs in challenge infection, results in a Th2 phenotype impairing parasite survival. This was confirmed by treatment of naïve mice with exogenous IL-25 and subsequent infection. Changes induced in goblet cell populations and mucin glycosylation could be implicated in resistance to infection.
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spelling pubmed-50342612016-09-29 Interleukin-25 Induces Resistance Against Intestinal Trematodes Muñoz-Antoli, Carla Cortés, Alba Santano, Rebeca Sotillo, Javier Esteban, J. Guillermo Toledo, Rafael Sci Rep Article Echinostoma caproni is an intestinal trematode that has been extensively used as an experimental model to investigate the factors determining the resistance to intestinal helminths or the development of chronic infections. ICR mice are permissive hosts for E. caproni in which chronic infections are developed, concomitantly with local Th1 responses, elevated levels of local IFN-γ, inflammation and antibody responses. However, mice develop partial resistance to homologous challenge infections after cure of a primary infection, which converts this subject into an adequate model for the study of the mechanisms generating resistance against intestinal helminths. The purpose of the present study was to compare the immune response induced in primary and secondary infections to elucidate the factors determining the different outcome of the infection in each type of infection. The results obtained indicate that susceptibility is determined by the lack of IL-25 expression in response to primary infection. In contrast, infection in an environment with elevated levels of IL-25, as occurs in challenge infection, results in a Th2 phenotype impairing parasite survival. This was confirmed by treatment of naïve mice with exogenous IL-25 and subsequent infection. Changes induced in goblet cell populations and mucin glycosylation could be implicated in resistance to infection. Nature Publishing Group 2016-09-23 /pmc/articles/PMC5034261/ /pubmed/27658962 http://dx.doi.org/10.1038/srep34142 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Muñoz-Antoli, Carla
Cortés, Alba
Santano, Rebeca
Sotillo, Javier
Esteban, J. Guillermo
Toledo, Rafael
Interleukin-25 Induces Resistance Against Intestinal Trematodes
title Interleukin-25 Induces Resistance Against Intestinal Trematodes
title_full Interleukin-25 Induces Resistance Against Intestinal Trematodes
title_fullStr Interleukin-25 Induces Resistance Against Intestinal Trematodes
title_full_unstemmed Interleukin-25 Induces Resistance Against Intestinal Trematodes
title_short Interleukin-25 Induces Resistance Against Intestinal Trematodes
title_sort interleukin-25 induces resistance against intestinal trematodes
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5034261/
https://www.ncbi.nlm.nih.gov/pubmed/27658962
http://dx.doi.org/10.1038/srep34142
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